essay on kidneys

Kidney: Structure, Function and Related Diseases

The structure of human kidney can be seen as two reddish bean-shaped organs that are located below the rib cage on each side of the spine. They are almost a fistful in size, measuring around 10-12cm. Kidneys are the main organs in the human excretory system, which takes part in the filtration of the blood before the urine is formed. Let us look at the structure of the organ for a better understanding.

External and Internal Features of Kidney

• It has a convex and concave border.
• Towards the inner concave side, a notch called the hilum is present through which the renal artery enters the kidney and the renal vein and ureter leave.
• The outer layer of the kidney is a tough capsule.
• On the inside, the kidney is divided into an outer renal cortex and an inner renal medulla.
• The hilum extends inside the kidney into a funnel-like space called the renal pelvis.
• The renal pelvis has projections called calyces(sing: calyx).
• The medulla is divided into medullary pyramids, which project into the calyces.
• Between the medullary pyramids, the cortex extends as renal columns called Columns of Bertini.
• The kidney is made up of millions of smaller units called nephrons which are also the functional units.

Read: Nephrons

A simple structure of kidney can be understood by the following diagram:

• The most important function of the kidney is to filter the blood for urine formation.
• It excretes metabolic wastes like urea and uric into the urine.
• Erythropoietin: It is released in response to hypoxia
• Renin: It controls blood pressure by regulation of angiotensin and aldosterone
• Calcitriol: It helps in the absorption of calcium in the intestines
• It maintains the acid-base balance of the body by reabsorbing bicarbonate from urine and excreting hydrogen ions and acid ions into the urine.
• It also maintains the water and salt levels of the body by working together with the pituitary gland .

Read: Urine Formation

Diseases related to Kidneys

In uremia, the kidneys are damaged, and there is a buildup of urea and other toxins in the blood, which is fatal and can cause kidney failure. Patients may experience fatigue, itching, muscle twitching, and loss of mental concentration. The urea can be removed by the process of hemodialysis.

2. Renal Calculi

Commonly called kidney stones, these are deposits of salt and minerals in our body. Symptoms include severe abdominal pain and nausea. The stones can be dissolved with medicines, or it passes with urine by improving diet and water intake.

3. Glomerulonephritis

It is the inflammation of the glomerulus. Symptoms include pink urine, oedema or swelling on the face and high blood pressure. It requires medical attention for prevention.

Note: Any person with high blood pressure and diabetes is more prone to kidney related diseases.

Explore BYJU’S Biology to learn more.

• Facts about Kidneys
• Regulation Of Kidney Function
• Kidney Function Test
• Kidney Failure Symptoms
• Difference Between Left and Right Kidney

What are the first signs of kidney problems?

You can see blood in your urine and it is also foamy. You will have a problem concentrating on things and will face swelling and dryness on your skin.

Can you live without a kidney?

It is not possible to live without a kidney. But since we have two of them, it is possible to survive with one kidney.

What causes kidney problems?

People with diseases like diabetes and high blood pressure have a high chance of developing kidney problems.

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• Review Article
• Published: 28 August 2012

The role of the kidney in regulating arterial blood pressure

• Hani M. Wadei 1 &
• Stephen C. Textor 2  

Nature Reviews Nephrology volume  8 ,  pages 602–609 ( 2012 ) Cite this article

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• Hypertension

The kidney plays a central role in the regulation of arterial blood pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal perfusion pressure are closely involved in maintaining the arterial circulation and blood pressure. Renal artery perfusion pressure directly regulates sodium excretion—a process known as pressure natriuresis—and influences the activity of various vasoactive systems such as the renin–angiotensin–aldosterone system. As a result, many researchers argue that identifying any marked rise in blood pressure requires resetting of the relationship between arterial blood pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood pressure. Results from studies of kidney transplantation indicate that pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension.

Renal artery perfusion pressure directly regulates sodium excretion, a process known as pressure natriuresis

The renin–angiotensin–aldosterone system has a central role in maintaining the pressure–natriuresis relationship

Maladaptive changes in tubular sodium and chloride handling leads to arterial hypertension despite the presence of a normal glomerular filtration rate

Rare inherited forms of hypertension involve gain or loss of function mutations in a single gene and are associated with increased sodium reabsorption in the distal nephron

Reduced nephron number contributes to the development of hypertension

The kidney is the origin of afferent sympathetic signalling that modulates the sympathetic nervous system, the activity of which increases in patients with renal failure

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Diabetic Renal Disease Essay

Introduction.

Diabetic renal disease also known as diabetic nephropathy is a medical condition which affects an individual’s blood sugar level as well as the kidney. This condition is characterized by persistence in albuminuria, reduced glomerular filtration rate and the increase in blood pressure within the arteries.

Research findings have shown that kidney disease is a complication that is associated with diabetes. Diabetic nephropathy has been a major course of kidney complications in those infected and a significant course of mortality. The disease is usually diagnosed after urinalysis and screening of the patient in relation to diabetes (Mogensen 2006, pp.640).

The albumiburia level is usually measured so as to determine whether the patient is affected by this condition. Early treatment is therefore very vital in preventing or delaying the onset of this condition. It particularly affects those patients who are affected by diabetes mellitus.

The high blood sugar levels in the patient usually result in the incapacitation of the kidney hence hindering the normal functioning of this organ. It becomes difficult for the kidney to filter blood hence resulting in full blown diabetes.

Under normal condition, the capillaries in the kidney are not damaged and hence act as filters to the unwanted substances in the blood. When these capillaries are damaged due to diabetes, these substances are not filtered and hence the impurities are retained in the blood (Lewis 2009).

The increase in blood glucose forces the kidney to filter much blood. When this condition persists over time the system collapses and blood proteins are passed to the urine a condition known as microalbuminuria. When this worsens, the condition is known as macroalbuminuria and this is characterized by huge amounts of proteins being found in the urine (Bennett 2005, p. 338-342).

The patient diagnosed with this complication is characterized by a number of signs and symptoms which include the dilation of the renal artery. The patient is likely to have fluid build-up, insomnia, general body weakness, loss of appetite, difficulty in concentration as well as stomach upsets.

When a laboratory test is carried out, such a patient is likely to have proteins in his/her blood. This is due to the damage caused on the capillaries in the kidney as evident in the specimen.

The system that helps in filtering the blood is damaged hence the blood proteins pass through the damaged capillaries into the urine. The patient is also likely to have an enlarged kidney as evident in the specimen. The risk of hypertension is quite high in this particular patient (Makita 2010, p. 963-975).

The patient with this condition is prone to cardiovascular diseases due to the damages caused on the blood vessels. This can be seen in the provided specimen as the blood vessels on the kidney appear to be swollen. Kidney failure is quite evident in the patient diagnosed with this condition.

The patient is also likely to pass urine that is full of foam. This is due to the high protein as well as glucose levels in the urine. The patient is also likely to have blurred vision.

This is caused by the damages on the blood vessels. Those blood vessels at the back of the eye or the retina are not spared. Once they are damaged, they start bleeding and hence cause the patient to have a blurred vision and in severe cases blindness might occur.

The patient is also likely to experience the narrowing of the arteries that lead to the kidney and have skin ulcers that take too long to heal. The patient is prone to peripheral nerve dysfunctions. The hypertension is basically due to the narrowing of the artilleries. There is poor circulation of blood in the blood vessels hence causing high blood pressure and hypertension (Brenner 2012, p. 4777).

The skin ulcers that take too long to heal are caused by the damage that occurs on the blood vessels. It therefore becomes difficult for the white blood cells to be transported to these areas. The concentration of antibodies in these areas is very low hence the difficulty in the healing of these ulcers.

Kidneys of a person affected by diabetes nephropathy retain excessive water and salts in the blood. This in the end results in increased blood pressure and hypertension. The excessive fluids are trapped within the body organs hence causing facial and leg swelling. The blood vessels in the specimen appear to be swollen which is primarily caused by the retention of excessive fluids by these vessels (Levey 2004, p.40-51).

The kidney in this specimen appears to be severely damaged hence its inability to perform the normal function of filtering impurities from the blood. The patient is therefore likely to have form in his/her urine due to the inability of the kidney to retain blood proteins and glucose within the blood.

The same is therefore passed to the urine. Hypertension is also caused by the fact that precipitated proteins are deposited in the blood vessels. The patient is also prone to conditions such as anemia, bone diseases and acidosis. In a normal person, the kidney is able to process the proteins in the blood unlike the diabetic person whose proteins cannot be synthesized hence are released into the urine.

The microvascular inflation is quite evident in diabetic patients as evident in the specimen provided. Most of the blood vessels are inflated due to the precipitation of protein particles on the membranes of these vessels (Watkins 2006, p. 293).

This particular patient is also prone to edema. This is a condition characterized by the swelling of the legs. The major cause of this is the retention of the interstitial fluid. The fluid is secreted into the interstitium and it is not easily drained away hence causing the legs to swell.

Edema is also caused by the biochemical and structural changes that are witnessed in the blood capillaries in the kidney as evident in the specimen shown. The vessels are made more permeable hence making it easier for the fluid to go through and be retained in the body tissues hence causing edema.

The tissues and blood vessels in the specimen appear to be swollen. This is due to the retention of excess water within these tissues hence causing the swelling (Hasslacher 2005, pp.234).

This patient suffering from the diabetic nephropathy is also likely to be witness an increase in weight. This is caused by the continued retention of fluid blood into the system hence causing the body to gain more weight (Ritz 2009, p. 302).

There are several remedies aimed at the prevention or slowing down of the diabetic kidney disease. One of the ways for the prevention of this condition is the intake of drugs that reduce the blood pressure. These drugs are aimed at protecting the kidney glomeruli and lower protenuria hence protein molecules are not passed to the urine. The most widely used drug is the lipsinopril (Selby 2009, p. 33).

Angiotensin Receptor Blockers are also used with the intension of ensuring the normal functioning of the kidney and lowering the wearing down of capillaries within the kidney hence slowing down the effects of the diabetic renal disease. Antihypertensive medicine is therefore very important in such a case.

It is also recommended that patients with this condition consume foods that are low in protein levels so as to prevent the onset of the kidney failure. Glycemic control is also quite crucial in the prevention or slowing down of this condition.

Patients with this condition are prone to high sugar or glucose levels hence the need to control the same. Insulin is quite important in the conversion of this glucose to energy and when the body does not respond to the insulin produced the same accumulates in the blood vessels hence causing hypertension (Whelton 2012, pp. 113).

Monitoring and controlling of blood sugar levels is very important in the prevention of this condition. In some cases, it might be necessary to administer insulin after meals or after intensive body activity so as to ensure that the ingested food is converted to glucose and broken down to produce the energy required by the body so as to avoid the build-up of glucose in the blood stream.

In cases where the disease has become full blown, dialysis and kidney transplant is the best remedy. Dialysis is quite vital in cleaning impurities out of ones blood in cases where the kidneys have failed. The blood is usually pumped out of the body and passed through a special filter that removes the impurities and it is then returned to the blood stream (Bakris 2012, p. 919).

The patients with diabetic renal disease need to keep their glucose levels at less than 7 percent and this can only be achieved through continuous check-ups. Insulin injection, issuing of the appropriate medication and proper diet are quite crucial in this case.

Physical Exercise is also important in such patients so as to facilitate the conversion of ingested food to glucose which is broken down for the provision of energy to the body. Appropriate measures should be taken to maintain low blood pressure of not more than 130/80. It is also important to measure the efficiency of the kidney by determining the protein levels in the urine.

For such patients, it is important to ensure that the average blood glucose is maintained at 155 mg%. Diabetic nephropathy patients who have been well taken care of should have lower cholesterol levels in their blood and reduced blood pressure which also reduces the risk of hypertension (Bojestig 2008, pp. 259).

The Metabolic Syndrome and obesity is mostly associated with the failure of the kidney to respond to insulin. The condition prevents the normal functioning of insulin particularly in the conversion of food into glucose and further breakdown of the same for the production of the energy for the body. The condition t leads to an increase in the glucose levels in the blood.

The blood vessels are blocked hence leading to high blood pressure. The most affected are the people who do not exercise, those who take in food rich in glucose/sugar and those on a high-protein diet.

These conditions are quite conducive for one to become diabetic hence the need for people to check their diets and lifestyle. An increase in people with the metabolic syndrome and obesity would imply an increase in people developing diabetic complications (Ziyadeh 2006, p.103).

Diabetic Nephropathy Kidney Specimen

List of References

Bakris, G. 2012, ‘Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy,’ Kidney International , vol. 33 no. 1, pp. 919.

Bennett, P. 2005, ‘Prevention of diabetic renal disease with special reference to microalbuminuria,’ Med Pub , vol. 15 no. 5, pp. 338-342.

Bojestig, M. 2008, ‘Declining incidence of nephropathy in insulin-dependent diabetes mellitus,’ New England Journal of Medicine , vol. 44 no. 5, pp. 359.

Boner, G. 2003. Management of Diabetic Nephropathy. New York: Taylor & Francis.

Brenner, B. 2012, ‘Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy,’ Hypertension and Chronic Kidney Disease Progression , vol. 20 no. 2, pp. 4777.

Hasslacher, C. 2005. Diabetes and the Kidney. London: John Wiley & Sons.

Levey, A. 2004, ‘The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease,’ American Journal of Transplantation, vol. 38 no. 8, pp. 40-51.

Lewis, J. 2009, ‘The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy,’ Journal of Renal Care,’ vol. 33 no. 2,pp. 4-11.

Makita, Z. 2010, ‘Mechanism of endothelial dysfunction in chronic kidney disease,’ The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, vol. 9 no. 6, pp. 963-975.

Mogensen, C. 2006, ‘The stages in diabetic renal disease: With emphasis on the stage of incipient diabetic nephropathy,’ diabetic nephropathy , vol. 10 no. 4, pp. 640.

Ritz, E. 2009, ‘Diabetic nephropathy in type II diabetes.’ American Journal of Kidney Diseases , vol. 12 no. 5, pp. 303.

Selby, J. 2009, ‘The natural history and epidemiology of diabetic nephropathy,’ The Journal of American Medical Association , vol. 5 no. 3, pp. 47.

Watkins, P. 2006, ‘Progression of nephropathy in long-term diabetics with proteinuria and effect of initial anti-hypertensive treatment,’ Scandinavian Journal of Clinical & Laboratory Investigation , vol. 1, pp. 293.

Whelton, P. 2012, ‘Blood pressure and end-stage renal disease in men,’ International Journal of Cardiology , vol. 8 no. 2, pp. 1113.

Ziyadeh, N. 2006, ‘The extracellular matrix in diabetic nephropathy,’ American journal of kidney diseases , vol. 1, no 1.pp103.

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By targeting high blood pressure, USF Health research on kidneys could also help your heart

• Dave Scheiber
• April 15, 2024

Morsani College of Medicine , Research

You would be hard-pressed to find a researcher who knows more about kidneys than USF Health’s Alexander “Sasha” Staruschenko, PhD. But the heart of his impactful renal work over the past two years reveals a potentially exciting cardiovascular benefit – in the form of an over-the-counter remedy with potentially far-reaching significance.

This potential remedy is a common and inexpensive amino acid called lysine – often sold in tablet form to reduce anxiety, prevent cold sores, improve calcium absorption and promote wound healing. The work of Dr. Staruschenko and his fellow researchers points to possible life-changing use: reducing kidney damage and high blood pressure.

“One of our main discoveries is that lysine – an essential amino acid – is critical for normal kidney function,” said Dr. Staruschenko, a professor of Molecular Pharmacology and Physiology and director of the Hypertension and Kidney Research Center in the USF Health Morsani College of Medicine.

And why should you care? Because your kidneys are far more critical to your overall health than many people realize – as Dr. Staruschenko points out. 

“Let’s start with why we need kidneys,” he said. “Many people probably think that kidneys are not that important. They’re not the heart, brain, or other vital organs. We have two kidneys, so who cares, right? But in reality, the kidney plays an important role in controlling your blood pressure (of course, together with other organs). Our research revealed that lysine might be beneficial for proper kidney function, thus helping to maintain normal blood pressure.”

Dr. Staruschenko and an international research team detailed these findings in the science journal Nature Communications in a paper entitled, “ Accelerated lysine metabolism conveys kidney protection in salt-sensitive hypertension .” Dr. Staruschenko served as the senior author. 

He is past chair of the Kidney in Cardiovascular Disease Council of the American Heart Association, deputy editor of the American Journal Physiology: Renal Physiology, and his research has been recognized nationally with a multitude of honors, including the American Society of Nephrology Distinguished Researcher Award. Meanwhile, his busy lab is dedicated to gaining a greater understanding of the role kidneys play in blood pressure control and chronic kidney disease (CKD).

Given that one in 10 people in developed countries suffer from kidney diseases – and that one-third of CKD cases are caused by hypertension – the lab’s work is paramount.

Kidneys, Dr. Staruschenko explains, maintain constant levels of electrolytes such as sodium, potassium, and calcium and use specialized ion channels to transport and regulate these minerals. Some channels are able to control blood pressure, which is a key area of his study since high blood pressure and diabetic kidney disease, a form of CKD, are the leading causes of kidney failure in the U.S.

That’s why his research and the results of this paper raise hopes for new avenues of treatment. The study demonstrated that taking lysine effectively protects the kidneys and prevents hypertension. While most experiments were conducted in a rat model, a small pilot study also pointed to similar results in humans.

That does not mean people should run out and buy bottles of lysine from the nearest drug or health food store. It only underscores that trials with rodents have yielded encouraging signs, but more testing is needed with humans and other rodent models to determine the depth of lysine’s effectiveness. One of the key factors in the research involves two different forms of hypertension: salt-resistant and salt-sensitive. 

“All of us consume more salt than is recommended, but some respond to it more than others,” Dr. Staruschenko explained. “Some individuals who are salt resistant can consume a higher level of sodium in their food and maintain normal blood pressure. It’s about half the people – the other half are salt-sensitive and can develop hypertension from extensive salt intake.”

That is where the promising benefits of lysine come in. “We specifically show that lysine is protective in salt-sensitive hypertension,” he said. “When it’s given to rodents with salt-induced hypertension, it prevents the progression and magnitude of hypertension.”

The key now, Dr. Staruschenko said, is obtaining more funding to expand the research, as well as to do a pilot study that would include more clinical testing involving humans. Some collaborators, in fact, have already started recruiting patients for new studies.

“Academic research cannot survive without funding; everything is very expensive in biomedical research,” he said. “Regarding this project, the industry is not interested in this particular study, because it’s a supplement that’s available over the counter. Thus, they can’t get a patent and make any money.” Therefore, federal, non-profit, or philanthropic organizations could support such lines of investigation.

In the meantime, his affiliation with the U.S. Department of Veterans Affairs and work benefitting veterans with kidney disease has led to valuable financial assistance.

“I was able to get a VA Merit Award, which has supported this line of research,” he said. “It is very relevant to veterans – these are people who are susceptible to hypertension, people with diabetes, people on dialysis, and people with different degrees of kidney function.  The fact is that the cost of dialysis alone is almost equivalent to the entire budget of the National Institutes of Health, the primary federal funding agency for biomedical and health-related research in the United States..”

Dr. Staruschenko is originally from St. Petersburg, Russia, which gave its name to St. Petersburg, Florida. His research career began when he completed his PhD in cell biology at the Institute of Cytology, Russian Academy of Science, in 2003. He considered continuing his education in Russia or perhaps Europe, but instead decided to make a major leap and come to the United States. He had never been to America, so he decided to make an exploratory visit, spending three weeks seeing New York, Washington, D.C., San Francisco and Dallas. “After that trip, I thought, ‘I can live and work in this country,’ ” he said. 

Not long after that, he received an offer from the University of Texas Health San Antonio to do his post-doctoral fellowship. Communication was an issue at first, given his thick Russian accent and his supervisor’s Texas drawl.  “We realized quickly that he didn’t understand me, and I didn’t understand him, so we initially communicated by email only,” he said. “Eventually, we were able to talk to each other, and at some point, he said, ‘Sasha, if you can understand me, you’ll be able to understand everyone!’ ”.

After four productive years, Dr. Staruschenko was hired as an assistant professor in 2007 at the Medical College of Wisconsin, eventually becoming a full professor in 2017. But after nearly 14 years, he was ready for a change, which came in the form of an offer to come to USF Health in 2021 in his dual role as professor and director of the Hypertension and Kidney Research Center. One year later, he co-authored the paper on the role of lysine, which received extensive media coverage in the U.S. and overseas.

“I was very pleased with that, but what’s most important is to see additional research in this area – and not only from my lab or my collaborators,” he said. “I want to see other researchers exploring this area. It is not about receiving credits or recognition. It is about moving this area forward.”

-- Photo and video by Allison Long, USF Health News 

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Home — Essay Samples — Nursing & Health — Kidney — Kidney dialysis

Kidney Dialysis

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Published: Mar 1, 2019

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Works Cited:

• Committee on the Rights of the Child. (2007). General comment No. 11: Indigenous children and their rights under the Convention.
• Committee on the Rights of the Child. (2011). General comment No. 13: The right of the child to freedom from all forms of violence.
• Committee on the Rights of the Child. (2013). General comment No. 17: The right of the child to rest, leisure, play, recreational activities, cultural life and the arts (art. 31).
• Committee on the Rights of the Child. (2014). General comment No. 15: The right of the child to the enjoyment of the highest attainable standard of health (art. 24).
• Committee on the Rights of the Child. (2016). General comment No. 20: On the implementation of the rights of the child during adolescence.
• Committee on the Rights of the Child. (2017). General comment No. 19: Public budgeting for the realization of children’s rights (art. 4).
• Committee on the Rights of the Child. (2019). General comment No. 24: Children’s rights in the child justice system.
• Committee on the Rights of the Child. (2020). General comment No. 18: On harmful practices.
• Convention on the Rights of the Child. (1989). United Nations Treaty Collection.
• Office of the High Commissioner for Human Rights. (2003). International human rights standards for law enforcement: A pocket book on human rights for the police.

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Chronic kidney disease in patients with diabetes mellitus

Espen nordheim.

1 Department of Transplantation Medicine, Section of Nephrology, Oslo University Hospital, Rikshospitalet, Oslo, Norway

2 Faculty of Medicine, University of Oslo, Oslo, Norway

Trond Geir Jenssen

3 Metabolic and Renal Research Group, Faculty of Health Sciences, UiT- The Arctic University of Norway, Tromsø

Chronic kidney disease is a common complication and concomitant condition of diabetes mellitus. The treatment of patients with diabetes and chronic kidney disease, including intensive control of blood sugar and blood pressure, has been very similar for type 1 and type 2 diabetes patients. New therapeutic targets have shown promising results and may lead to more specific treatment options for patients with type 1 and type 2 diabetes.

Introduction

Diabetes mellitus is among the leading causes of chronic kidney disease and end-stage kidney disease in the western world. It was the most common diagnosis for the initiation of renal replacement therapy in the United States in 2018, accounting for 47% of the cases ( 1 ).

Type 1 and type 2 diabetes mellitus share many clinical characteristics and long-term complications, but they are in fact two different diseases with diverging pathophysiology ( 2 ). While type 1 diabetes results from autoimmune destruction of the insulin-producing beta-cells within the pancreatic islets of Langerhans, type 2 diabetes is most often characterized by insulin resistance together with insufficient insulin response, at least in White people.

Type 1 and type 2 diabetes mellitus can both cause long-term microvascular and macrovascular complications, contributing to the increased morbidity and mortality among these patients. Kidney disease in patients with diabetes can be a result of microvascular complications from diabetes, a concomitant kidney disease of other origin or a combination of the two. In type 1 diabetes patients, microvascular disease secondary to diabetes is the most common etiology to chronic kidney disease, while a spectrum of etiologies can cause kidney disease in type 2 diabetes patients.

The established treatment principals to prevent and halt progression of chronic kidney disease have been very similar in the two diabetic phenotypes. This review article intends to highlight the established and upcoming treatment for patients with type 1 and type 2 diabetes and chronic kidney disease. We have reviewed landmark papers published up till the fall of 2020 and publications dealing with new potential therapeutic targets. This review is based on literature search in Pubmed with the following combinations of keywords: 'diabetic nephropathy', 'diabetic kidney disease', 'diabetic nephropathy treatment' and 'diabetic kidney disease treatment' to complete our own bibliography. The search yielded a total of 79.367 search results and was closed on October 26, 2020. The relevance of the articles was initially assessed on the basis of title and abstract before relevant articles in English language were read in full text. Reference lists of all articles read were analyzed in order to identify reference articles for the review.

Kidney disease in patients with type 1 diabetes mellitus

Type 1 diabetes usually affects young and middle-aged patients and among these patients, chronic kidney disease is most often caused by diabetes-related microvascular disease ( 3 ), a condition which has been referred to as diabetic nephropathy or 'diabetic kidney disease' in the literature.

Chronic kidney disease in type 1 diabetes patients typically can cause a progressive decline in renal function. Hyperglycaemia starts the pathophysiologic mechanisms with a subsequent interplay of altered haemodynamics, metabolic and inflammatory pathways ( 4 ). When glomerular foot processes merge and the integrity of the glomerular basement membrane is compromised by pathological processes, albumin and subsequently, larger proteins can leak into the urine. Urine albumin/creatinine ratio (UACR) spot analysis of first morning collection is preferred for proteinuria quantification, above assessment of albumin in 24 h urine collection. UACR are staged into moderate albuminuria, previously called microalbuminuria (30–300 mg/g) and overt albuminuria, previously called proteinuria (≥300 mg/g).

Chronic kidney disease in type 1 diabetes patients is initially characterized by hyperfiltration due to increased glomerular filtration pressure ( 5 ). Cherney et al . postulated hyperglycaemia-dependent hyperfiltration to be mediated through upregulated back-transportation of sodium and glucose from the renal tubular system ( 6 ). Sodium-glucose-co-transporter-2 (SGLT2) contributes to 90% of this transportation reducing distal tubular flux of glucose and sodium. Due to reduced sodium flux in the loop of Henle, macula densa signals dilatation of the afferent arteriolar tone through a tubuloglomerular feedback mechanism which increases tubular sodium flux at the expense of increase of intraglomerular pressure and hyperfiltration at the nephron level. Hyperfiltration is in the clinic seen as an increase in glomerular filtration rate (GFR) ( 5 , 6 ). Albuminuria and hypertension subsequently occur as the kidney disease develops. After the initial hyperfiltration phase, nephrons are lost resulting in a steady GFR decline ranging 3–6 mL/min/year ( 4 ). Renal failure requiring replacement therapy may eventually occur within 20–25 years. During this process, the remaining nephrons compensate by hyperfiltration not only due to hyperglycemia but now also due to reduced total filtration surface. This represents a vicious circle with progressive loss of nephrons.

In his first model of the disease, Mogensen suggested that the pathological processes in chronic kidney disease in type 1 diabetes patients were irreversible and that the disease gradually progressed ( 5 ). Later, this model has been challenged by reports describing that renal function may be reduced without concomitant proteinuria and that proteinuria may cease spontaneously in the course of the disease ( 7 ). These reports used estimated GFR based on cystatin c measurements, and they have, thus, been challenged since these estimates of GFR may differ substantially from measured GFR ( 8 ).

Kidney disease in patients with type 2 diabetes mellitus

While chronic kidney disease in type 1 diabetes most often is secondary to diabetes microvascular disease, there is a whole spectrum of chronic kidney disease etiologies in type 2 diabetes. Type 2 diabetes patients are often older at the time of diagnosis and kidney disease due to other causes than diabetes is likely to occur. Several studies have verified that kidney disease in type 2 diabetes may be a more compounded entity than what is seen in type 1 diabetes ( 9 ). One study from the United States which examined kidney biopsies in patients with type 2 diabetes and kidney disease found that typical diabetic microvascular disease were present in 37% of the cases, non-diabetic kidney disease in 36% of the cases, such as nephrosclerosis or immunological kidney disease, while mixed forms of diabetic and non-diabetic kidney disease were found in 27% of the cases ( 10 ). Interestingly, one study has found different insulin resistance phenotypes in diabetes to be associated with different risks for chronic kidney disease ( 11 ), but this needs to be studied further.

Regardless of kidney disease etiology, strict blood glucose control is on a group level the single-most important intervention to prevent kidney disease to develop in patients with type 1 and type 2 diabetes ( 12 , 13 , 14 ). Normalization of blood glucose might act renoprotective through different mechanisms: reduced hyperfiltration on the nephron level ( 15 , 6 ), reduced generation of toxic intermediates such as reactive oxygen species (ROS) ( 16 ) and reduced activity in pathogenetic signalling pathways including the polyol, hexasamine, protein kinase C and advanced glycation end-product pathways ( 17 ).

Still as the chronic kidney disease progresses, GFR is reduced through nephron loss and hyperfiltration in remaining nephrons drives the process further.

How to diagnose kidney disease in patients with diabetes?

Typically, patients with established diabetes are diagnosed with kidney disease when albuminuria is identified as elevated in two out of three spot urine analyzes, corresponding to urine albumin/creatinine ratio (UACR) at or above 30 mg/g and/or persistently impaired renal function, defined as estimated glomerular filtration rate (eGFR) below 60 mL/1.73 m 2 .

Our clinical impression is that, in most cases, patients with diabetes are not referred for diagnostic kidney biopsy when kidney disease is verified, especially if the clinical characteristics do not differ from what can be expected from chronic kidney disease in diabetes (i.e. increased albuminuria, hypertension and slow decrease in estimated GFR). However, other diseases must be suspected when no other microvascular complications of diabetes are present and also in the presence of microscopic haematuria ( 9 ). The pathological classification system developed for chronic kidney disease in type 1 diabetes also includes type 2 diabetes ( 3 ). It has been argued that a common classification system is challenging due to the differences in renal lesions among the two diseases ( 18 ). While type 1 diabetes patients typically have glomerular lesions characterized by thickening of the glomerular basement membrane, mesangial expansion and glomerulosclerosis, only 30% of type 2 diabetes patients with microalbuminuria and 50% with proteinuria demonstrate such lesions ( 19 ).

Established treatment of chronic kidney disease for type 1 and type 2 diabetes

Intensive blood sugar control.

Long-term hyperglycaemia causes glomerular hyperfiltration together with glycation of cell proteins, especially intranuclar proteins and nucleic acids. Intensified blood sugar control reduces the risk for proteinuria to develop and also to progress ( 12 , 13 , 14 ). Prevention of overt proteinuria is beneficial for maintaining renal function over time ( 12 , 13 , 14 ). The effect is well-documented in patients with type 1 diabetes ( 12 , 13 ) and has also been demonstrated at a group level for patients with type 2 diabetes ( 14 ). Most guidelines recommend glucose control corresponding to HbA1c around 53 mmol/mol (7%), provided good quality of life is maintained without causing repeated or even severe episodes of hypoglycaemia ( 20 , 21 ).

The risk for severe hypoglycaemic episodes increases when GFR falls below 45 mL/min. Hypoglycaemic episodes may develop due to reduced gluconeogenesis and counter-regulation in the kidneys ( 22 ) and also the half-life of blood glucose-lowering drugs can be prolonged when renal function is impaired, which may necessitate dose-lowering or cessation of drugs such as insulin or sulfonylureas. The increased risk for metformin-related lactacidosis must also been taken into consideration when renal function is impaired ( 23 ).

Regulation of blood pressure and albuminuria is beneficial for chronic kidney disease in diabetes

Carl Erik Mogensen reported in 1976 on how blood pressure must be lowered in order to prevent decline in renal function in patients with type 1 diabetes ( 24 ). The treatment target for this patient group is blood pressure below 130/80 mmHg ( 25 , 26 ). Blocking of the renin-angiotensin-aldosterone (RAAS) system is particularly effective in order to reduce proteinuria and preserve renal function, regardless of the blood pressure, first demonstrated for captopril in patients with type 1 diabetes and nephropathy ( 27 ) and later for losartan and irbesartan in type 2 diabetes ( 28 , 29 ). Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) reduce intraglomerular filtration pressure by dilating the efferent glomerular arteriole, and the clinical effects of these two classes of drugs are considered as equivalent ( 30 ). If proteins are present in the urine, it is crucial to reduce the level of proteinuria in order to reduce the risk for kidney disease progression ( 31 ). To achieve a reduction of proteinuria, RAAS-blocking drugs are often needed in higher doses to reduce proteinuria than for reaching the blood pressure target alone ( 32 ). To be able to monitor and evaluate treatment effect, the amount of proteinuria should be quantified and followed with ACR in urine, which can be easily analyzed in spot samples of morning urine ( 33 ).

Other interventions beneficial for chronic kidney disease in diabetes

A comprehensive care is recommended for the management of diabetes patients in the recent KDIGO clinical practice guidelines ( 21 ), including statins to all patients with diabetes and kidney disease regardless of cholesterol levels to prevent cardiovascular disease. Moderate physical activity for at least 150 min per week is recommended in addition to smoking cessation, weight loss in the case of obesity, salt restriction and protein-reduced diet.

Recent studies on glucose-lowering treatment with clinical impact for patients with type 2 diabetes

Patients with type 1 diabetes need treatment with exogenous insulin to obtain blood glucose control, while type 2 diabetes patients might reach treatment targets with life-style modifications, with or without addition of oral glucose lowering agents. The last decade has presented a large selection of blood-glucose lowering drugs for type 2 diabetes patients, and it has been demonstrated that especially two classes of drugs have particular beneficial effects in patients with kidney disease beyond the blood-glucose lowering effect: receptor agonists of the glucagon-like protein 1 receptor (GLP-1 RA) and inhibitors of sodium-glucose-co-transporter-2 (SGLT2i). In secondary analyses of the SAVOR-TIMI 53 and CARMELINA studies, the dipeptidyl peptidase-4 inhibitors (DPP4i) – saxagliptin and linagliptin were associated with less development of macroalbuminuria ( 34 , 35 ) but with no effect on major cardiovascular endpoints ( 36 , 35 ). However, the antiproteinuric effect is more pronounced with GLP-1 RAs. Renal outcomes were included in six out of the major GLP-1 RAs studies on cardiovascular outcome (CVOT): lixisenatide (ELIXA), liraglutide (LEADER), semaglutide (SUSTAIN-6), exenatide (EXSCEL), dulaglutide (REWIND and AWARD-7) ( 37 , 38 , 39 , 40 , 41 , 42 ). Major adverse cardiovascular events and death were the primary outcomes of all these studies, while composite renal endpoints were among the secondary outcomes. The renal endpoints were not standardized, but all included proteinuria and change in estimated GFR. Lixisenatide, liraglutide, semaglutide, exenatide and dulaglutide all seemed to demonstrate a protective effect on composite renal outcomes. This effect was apparently driven by reduced development of macroalbuminuria and not by stabilization of GFR ( 37 , 38 , 40 ). However, dulaglutide seemed to preserve renal function better compared to insulin glargine after 1 year of treatment in patients with type 2 diabetes in AWARD-7 ( 42 ).

How GLP-1 RAs provide beneficial effects in the kidneys, outside lowering of blood glucose, is not fully understood. It has been suggested that GLP-1 agonism mediates reduced inflammation and oxidative stress. GLP-1 RA increases natriuresis, probably by inhibiting sodium/hydrogen isoform 3 (NHE3) in the renal tubules ( 43 ), but the renal haemodynamic effects seem neutral as the drug also causes glomerular vasodilatation ( 44 ). Weight loss, another known effect of GLP-1 RA leading to reduced hyperfiltration and improved proteinuria, might also have a role.

Promising results were found with the SGLT2-inhibitors early in the cardiovascular safety studies, for example, with empagliflozin (EMPA-REG), canagliflozin (CANVAS) and dapagliflozin (DECLARE- TIMI 58) ( 45 , 46 , 47 , 48 ). Composite renal outcomes were studied as secondary endpoints also in these studies, and it was observed that SGLT2i not only seemed to reduce proteinuria but also to delay deterioration of renal function (eGFR).

How can we understand the SGLT2i effects in chronic kidney disease?

SGLT2-mediated retention of glucose in the kidneys is probably a calorie saving mechanism which enabled survival in times when access to exogenous energy resources were more restricted than today. In a normal diet, the kidneys reabsorb 180 g glucose (720 kilocalories) daily. During diabetes and hyperglycaemia, the reabsorption of glucose and sodium is increased even more and less sodium is presented to macular densa distal to loop of Henle. This in turn initiates a tubuloglomerular feedback mechanism which dilates the afferent arteriole leading to an increase in GFR. Thus, tubular sodium flux is reestablished at the expense of hyperfiltration which is detrimental for the glomerular tuft in the long run.

The excretion of sodium into the urine increases due to the co-inhibitory effect of SGLT2i, which again normalizes the afferent arteriole tone through its effect on macula densa ( 6 ). Increased afferent arteriole tone translates into a reduced filtration pressure in the glomeruli and, thus, reduced load on the glomerular tuft. Additional potential beneficial mechanisms of SGLT2i may be increased oxygenation of tubular cells, possible reduction of toxic effects on renal tubules secondary to reduced albuminuria, preservation of intravascular volume and reduced volume overload due to loop-diuretic sparing effect in addition to improved metabolic parameters (i.e. body weight and HbA1c) ( 49 ). One study found post-glomerular vasodilatation of the SGLT2 inhibitor dapagliflozin rather than pre-glomerular vasoconstriction in metformin-treated patients with type 2 diabetes ( 50 ).

The CREDENCE study was the first study that primarily included type 2 diabetes patients with kidney disease ( 51 ). This was a randomized placebo-controlled trial of more than 4000 type 2 diabetes patients with estimated glomerular filtration rate (eGFR) between 30 and 90 mL/min/1.73 m 2 and UACR ranging 300–5000 mg/g. The pre-specified efficacy criteria for the study were achieved earlier than expected and led to an early termination of the study ( https://www.jnj.com/phase-3-credence-renal-outcomes-trial-of-invokana-canagliflozin-is-being-stopped-early-for-positive-efficacy-findings ; accessed October 26, 2020). After a median follow-up of 2.6 years, the treatment group had a significant reduction in the combined renal-specific endpoint (development of terminal kidney failure, doubling of serum creatinine or death from renal-specific cause). These results were valid also for the patients with the most reduced renal function in the study. In fact, in a subset of patients with a GFR drop to less than 30 mL/min/1.73 m 2 just prior to randomization, safety and efficacy of the drug was in line with the whole study population ( 52 ). Renoprotective effects occur at GFR thresholds where glucose lowering is no longer observed. The ability for SGLT2i to lower blood glucose decreases sharply when estimated GFR falls below 60 mL/min/1.73 m 2 ( 53 ), while the CREDENCE study documented kidney protective effects in the patient group with estimated GFR ranging from 30 to 45 mL/min/1.73 m 2 and even lower.

The DAPA-CKD study studied whether the SGLT2 inhibitor dapagliflozin could have beneficial renal effects also in non-diabetic patients with chronic kidney disease (CKD). Due to superior effects on the renal endpoints, the study was halted before scheduled time ( 54 ). The study involved 4.304 patients with CKD out of which only 68% had type 2 diabetes, and the primary end-point was: decline in the estimated GFR of at least 50%, end-stage kidney disease, or death from renal or cardiovascular causes. Patients with eGFR down to 25 mL/min/1.73 m 2 were included. The study found significant reduction in the primary endpoint and the effect was found independently of presence of diabetes. The number of patients needed to be treated to prevent one incident was as low as 19 during follow-up (median 2.4 years). The EMPEROR-Reduce study, published simultaneously, studied the effect of empagliflozin in heart failure patients already on RAAS blockage and found that empagliflozin was superior to placebo in preventing cardiovascular death or hospitalization for heart failure ( 55 ). Rate of eGFR decline was a secondary outcome of the study. The annual decline in eGFR was slower in the empagliflozin group compared to the placebo group (0.55 mL/min/1.73 m 2 vs 2.28 mL/min/1.73 m 2 ). The DAPA-HF trial studied the effect of dapagliflozin in heart failure patients and found a lower risk of heart failure worsening or death from cardiovascular causes in the treatment group compared to placebo, regardless of the presence of absence of diabetes ( 56 ). The incidence of the prespecified renal composite outcome did not differ between the treatment groups. The number of patients with kidney disease in the DAPA-HF trial was low which may have reduced the power to detect statistically significant differences.

The VERTIS study could not demonstrate a significant effect of ertugliflozin on the primary major adverse cardiovascular events endpoint, but the results showed numerically beneficial outcome for preservation of GFR compared to placebo ( 57 ). Table 1 summarizes the recent SGLT2i studies with demonstrated effects on renal endpoint.

Summary of recent SGLT2i studies with effects on primary and secondary renal endpoints.

The ongoing EMPA-KIDNEY study also addresses the renal outcome of using the SGLT2 inhibitor empagliflozin in persons with CKD. In this study also patients with type 1 diabetes are included, in addition to patients with type 2 diabetes or no diabetes (ClinicalTrials.gov. {"type":"clinical-trial","attrs":{"text":"NCT03594110","term_id":"NCT03594110"}} NCT03594110 ). The study plans to recruit in total 5000 patients including type 1 diabetes, type 2 diabetes and non-diabetic patients with impaired renal function (eGFR ≥ 20 to <45 mL/min/1.73 m 2 or eGFR ≥ 45 to <90 mL/min/1.73 m 2 and UACR ≥ 200 mg/g) and the results are estimated to be published by summer 2022.

In the 2020 KDIGO guidelines for diabetes management in chronic kidney disease, the combination of metformin and SGLT2i is now recommended as first line treatment for all type 2 diabetes patients with chronic kidney disease if eGFR is above 30 mL/min per 1.73 m 2 regardless of glucose control, even in patients with HbA1c within the target range. If the patient does not achieve the individualized glycaemic target, the addition of a GLP-1 RA is recommended ( 21 ). Previous and upcoming studies on SGLT2-inhibitors studies are all performed in patients already treated with RAAS blockage or inhibition. Thus, one might expect that current treatment with ACEi or ARBs will still be a basic therapy in the future.

Other therapeutic targets recently tested

Atrasentan, an endothelin A-receptor antagonist, was investigated in the SONAR study ( 58 ). Atrasentan is thought to have beneficial effects in several pathophysiological processes involved in chronic kidney disease in patients with diabetes, altered haemodynamics, inflammation and fibrosis. The study included type 2 diabetes patients with eGFR 25–75 mL/min/1.73 m 2 and UACR 300–5000 mg/g and demonstrated a lower reduction in eGFR and reduced proteinuria when compared to placebo. Another and smaller clinical study on pirfenidion, an inhibitor of TGF-β (transforming grown factor beta), included patients with both type 1 and type 2 diabetes with kidney failure and proteinuria and reported improvement in eGFR after 1 year treatment compared to placebo ( 59 ). Sulodexide, a glycosaminoglycan described as being able to prevent structural changes in the glomerular basement membrane, has shown positive effects on proteinuria in two small studies ( 60 , 61 ). Bardoxolone mathyl is demonstrated to improve inulin GFR in a Japanese phase 2 study, the phase 3 study results are expected early in 2022 ( 62 ). Lowering of the serum urate level with allopurinol was ,however, not shown to slow the decrease in the glomerular filtration rate (GFR) in persons with type 1 diabetes and early-to-moderate diabetic nephropathy ( 63 ). FIDELIO-DKD found promising results with finerenone, a selective mineralocorticoid, on diabetic nephropathy and cardiovascular endpoints ( 64 ).

Studies in progress

In addition to the EMPA-KIDNEY study which examines SGLT2i in type 1 diabetes patients, other studies are of potential interest. The FLOW trial (Semaglutide on the progression of renal impairment in subjects with type 2 diabetes and chronic kidney disease) is designed to show whether the GLP-1 RA semaglutide can slow the decline in eGFR among type 1 diabetes patients with chronic kidney disease. The trial is still recruiting patients and will evaluate when a sufficient amount of end-points has been obtained, alternatively after 5 years. The primary endpoint is persistent eGFR decline of >50%, reaching end-stage renal disease, death from kidney disease or death from cardiovascular disease (ClinicalTrials.gov identifier: {"type":"clinical-trial","attrs":{"text":"NCT03819153","term_id":"NCT03819153"}} NCT03819153 ).

FIGARO-DKD will give us more answers to the role of finerenone in the treatment of chronic kidney disease in type 1 diabetes patients and cardiovascular endpoints (ClinicalTrials.gov: {"type":"clinical-trial","attrs":{"text":"NCT02545049","term_id":"NCT02545049"}} NCT02545049 ). Another interesting study investigates whether reduced oxidative stress by inhibiting NADPH oxidase can reduce proteinuria and preserve renal function in patients with type 1diabetes and moderate renal failure ( 65 ).

The established treatment of diabetes patients with chronic kidney disease has up till now been very similar for type 1 or type 2 diabetes patients. Recent studies have, however, demonstrated that type 2 diabetes patients with impaired renal function have beneficial renal effects beyond the glucose- lowering effects of especially SGLT2i but also GLP-1 RA. Future studies will clarify if new drugs will arrive in the treatment of type 1 diabetes patients with chronic kidney disease.

Declaration of interest

EN has no conflict of interest that could be perceived as prejudicing the impartiality of the research reported. TGJ has received lecture fees from AstraZeneca, Mundipharma, Boehringer Ingelheim, and Novo Nordisk.

This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.