Established Chronic Kidney Disease – Chronic Renal Failure

Dr Nihal Kumar , BHMS (PUNE)

“The composition of the blood and internal environment is determined not by what the mouth ingests but by what the kidney keeps” 

Normal Kidneys and Their Function
The kidneys are a pair of bean-shaped organs that lie on either side of the spine in the lower middle of the back. Each kidney weighs about ¼ pound and contains approximately one million filtering units called nephrons. Each nephron is made of a glomerulus and a tubule. The glomerulus is a miniature filtering or sieving device while the tubule is a tiny tube like structure attached to the glomerulus.

The kidneys are connected to the urinary bladder by tubes called ureters. Urine is stored in the urinary bladder until the bladder is emptied by urinating. The bladder is connected to the outside of the body by another tube like structure called the urethra.

The main function of the kidneys is to remove waste products and excess water from the blood. The kidneys process about 200 liters of blood every day and produce about two liters of urine. The waste products are generated from normal metabolic processes including the breakdown of active tissues, ingested foods, and other substances. The kidneys allow consumption of a variety of foods, drugs, vitamins and supplements, additives, and excess fluids without worry that toxic by-products will build up to harmful levels. The kidney also plays a major role in regulating levels of various minerals such as calcium, sodium, and potassium in the blood.

  • As the first step in filtration, blood is delivered into the glomeruli by microscopic leaky blood vessels called capillaries. Here, blood is filtered of waste products and fluid while red blood cells, proteins, and large molecules are retained in the capillaries. In addition to wastes, some useful substances are also filtered out. The filtrate collects in a sac called Bowman’s capsule.
  • The tubules are the next step in the filtration process. The tubules are lined with highly functional cells which process the filtrate, reabsorbing water and chemicals useful to the body while secreting some additional waste products into the tubule.

The kidneys also produce certain hormones that have important functions in the body, including the following:

  • Active form of vitamin D (calcitriol or 1,25 dihydroxy-vitamin D), which regulates absorption of calcium and phosphorus from foods, promoting formation of strong bone.
  • Erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells.
  • Renin, which regulates blood volume and blood pressure. 

INTRODUCTION:- Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function over time. This happens gradually, usually months to years. Chronic kidney disease is divided into five stages of increasing severity (see Table 1 below). The term “renal” refers to the kidney, so another name for kidney failure is “renal failure.” Mild kidney disease is often called renal insufficiency.

With loss of kidney function, there is an accumulation of water; waste; and toxic substances, in the body, that are normally excreted by the kidney. Loss of kidney function also causes other problems such as anemia, high blood pressure, acidosis (excessive acidity of body fluids), disorders of cholesterol and fatty acids, and bone disease.

Stage 5 chronic kidney disease is also referred to as kidney failure, end-stage kidney disease, or end-stage renal disease, wherein there is total or near-total loss of kidney function. There is dangerous accumulation of water, waste, and toxic substances, and most individuals in this stage of kidney disease need dialysis or transplantation to stay alive. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF) 

Table 1. Stages of Chronic Kidney Disease

Stage Description GFR*
1 Slight kidney damage with normal or increased filtration More than 90
2 Mild decrease in kidney function 60-89
3 Moderate decrease in kidney function 30-59
4 Severe decrease in kidney function 15-29
5 Kidney failure Less than 15 (or dialysis)

*GFR is glomerular filtration rate, a measure of the kidney’s function. 

Established  chronic    kidney disease(chronic renal failure):-
Chronic renal failure is irreversible deterioration in renal function. Impairment in excretory, metabolic and endocrine functions of the kidney leads to the development of uremia. These patients usually have bilateral small kidneys. Renal failure of more than six months are termed as chronic.

The end result of many renal diseases — whether they are renal vascular diseases, glomerulonephritis, or chronic pyelonephritis–is end stage renal disease (ESRD). In ESRD, the kidneys are small bilaterally, as shown here. This condition is associated with chronic renal failure, and the patient’s blood urea nitrogen (BUN) and serum creatinine continue to increase. Chronic renal failure can be treated by dialysis or by kidney transplantation, as shown here. Note the normal size of the pre-owned kidney in comparison with native diseased kidneys.

The incidence rates of end-stage renal disease (ESRD) have increased steadily internationally since 1989. The United States has the highest incident rate of ESRD, followed by Japan. Japan has the highest prevalence per million population, with the United States taking second place.

Risk factors for developing CKD differ between races and countries.It would be interesting to know the incidence of CKD and itscauses in India, which is a densely populated country with lowincome, different food, cultural traditions and lifestyle habits.In contrast to high-income countries, patients with ESRD haveto pay for dialysis and transplantation themselves. The currentlyreported incidence of CRF in India is based on extrapolateddata from the US. As yet, no large-scale population studiesare available.

We conducted two studies:

(i)  a population screening in NewDelhi

(ii) a second prospective study that involved48 hospitals.

In the population screening 4712 subjects participatedin a blood biochemistry test. Mean age was 42.38±12.54years, 56.16% were male. Thirty-seven were found to have chronicrenal failure (prevalence rate of 0.78%). If these data areapplied to India’s 1 billion population there are 7.85 millionCRF patients in India. Aetiologically, diabetes (41%), hypertension(22%), chronic glomerular nephritis (16%), chronic interstitialdisease (5.4%), ischaemic nephropathy (5.4%), obstructive uropathy(2.7%), miscellaneous (2.7%) and unknown cause (5.4%) constitutedthe spectrum.

The second study was more representative, as 48 centres weredistributed all over India. Data were based on prospective investigationsconducted over a period of 1 (33 hospitals) to 3 months (15hospitals) comprising 4145 CKD patients. It showed the followingaetiological pattern: diabetes (29.7%), chronic glomerulonephritis(19.3%), hypertension (14%), chronic interstitial disease andvesico-ureteral reflux (12.6%), obstruction and calculus (9.3%),ADPKD and Alport Syndrome (8.4%), undiagnosed (6.2%). This studyshows that the prevalence of CRF in India is 0.8%. If we combinethe two, diabetes has emerged as the most frequent cause (30–40%)followed by hypertension (14–22%), CGN (16–20%),CIN (5.4–12.7%), heredofamilial disease (8.4%), obstructionincluding calculus (2.9%). The two studies, which are differentin some ways, perhaps explain the wide range in incidence, suggestingregional influences.

Prevalence and incidence of end-stage renal failure:-
Approximately 30% of patients with diabetic nephropathy eventually progress to end-stage renal failure, and the rest usually die from cardiovascular disease before reaching end stage. All develop microalbuminuria and, subsequently, proteinuria. Therefore, albuminuria is an important risk factor in these patients, and all diabetic patients should have a microalbuminuria assessment yearly9. Indeed, albuminuria is strongly associated with progression of kidney disease, in addition to prediction of cardiovascular events not only in diabetic patients, but also in the general community10,11. Thus, the combination of diabetes, hypertension, and chronic kidney disease is now the most common cause of end-stage kidney failure worldwide.

The incidence of patients with end-stage renal disease being treated by renal replacement therapy varies enormously depending on the level of affluence of the country. The highly developed countries such as North America, Europe, and Japan have the highest incident rates of treated end-stage renal failure, whereas the emerging countries have very low incident rates. There are now over 1 million dialysis patients worldwide, with an incidence of about a quarter of a million new patients each year.12 The annual incidence of new cases of end-stage renal failure in Hong Kong from their renal registry data demonstrates the worldwide trend of progressively increasing numbers. In 1996, there were 100 patients/million population beginning dialysis in Hong Kong. In the year 2000, this increased to 122 patients, and in 2003, 140 patients/million population began treatment for end-stage renal failure. Similarly, the rates have been increasing in the United States, and with increasing prevalence, it is predicted that by 2010, there will be almost 700,000 dialysis patients in the United States, costing about US$30 million a year for their dialysis treatment13. Obviously, treatment of such an ever-increasing burden of end-stage kidney failure cannot be afforded, even in the wealthiest of countries.

Mortality/ Morbidity:-
Among patients with ESRD aged 65 years and older, the mortality rates are 6 times higher than in the general population. In 2003, over 69,000 dialysis patients enrolled in the ESRD program died (annual adjusted mortality rate of 210.7 per 1000 patient-years at risk for the dialysis population, which represents a 14% decrease since peaking at 244.5 per 1000 patient-years in 1988). The highest mortality rate is within the first 6 months of initiating dialysis, which then tends to improve over the next 6 months, before increasing gradually over the next 4 years.

The mortality rates associated with hemodialysis are striking and indicate that the life expectancy of patients entering into hemodialysis is markedly shortened. At every age, patients with ESRD on dialysis have significantly increased mortality when compared with nondialysis patients and individuals without kidney disease. At age 60 years, a healthy person can expect to live for more than 20 years, whereas the life expectancy of a 60-year-old patient starting hemodialysis is closer to 4 years.

Choi et al found that rates of end-stage renal disease among black patients exceeded those among white patients at all levels of baseline estimated glomerular filtration rate (eGFR).1 Similarly, mortality rates among black patients were equal to or higher than those among white patients at all levels of eGFR. Risk of end-stage renal disease among black patients was highest at an eGFR of 45-59 mL/min/1.73 m2 (hazard ratio, 3.08), as was the risk of mortality (hazard ratio, 1.32).

In The Third National Health and Examination Survey (NHANES III), the distribution of estimated GFRs for the chronic kidney disease stages was similar in both sexes. Nonetheless, the United States Renal Data System (USRDS) 2004 Annual Data Report reveals that the incident rate of ESRD cases is higher for males with 409 per million population in 2002 compared to 276 for females.

Chronic kidney disease is found in persons of all ages. The normal annual mean decline in the GFR with age from the peak GFR (approximately 120 mL/min/1.73 m2) attained during the third decade of life is approximately 1 mL/min/y/1.73 m2, reaching a mean value of 70 mL/min/1.73 m2 at age 70 years. Nonetheless, in the United States, the highest incidence rate of ESRD occurs in patients older than 65 years. As per NHANES III data, the prevalence of chronic kidney disease was 37.8% among patients older than 70 years. Besides diabetes mellitus and hypertension, age is an independent major predictor of chronic kidney disease.

Chronic renal failure may be caused by any condition that destroys the normal structure and function of the kidney. Common causes are;

1. Congenital and inherited diseases:

  • Polycystic kidney disease (infantile or adult)
  • Alport’s syndrome
  • Congenital hypoplasia

2. Vascular diseases

  • Arteriosclerosis
  • Vasculitis (PAN, SLE, scleroderma)

3. Glomerular diseases

  • Proliferative Glomerulo nephritis
  • Crescentic Glomerulo nephritis
  • Membranous Glomerulo nephritis
  • Mesangio capillary Glomerulo nephritis
  • Glomerulosclerosis
  • Secondary Glomerulo nephritis

4. Interstitial diseases:

  • Chronic Pylonephritis
  • Vesico- ureteric reflux
  • Tuberculosis
  • Analgesic nephropathy
  • Nephrocalcinosis
  • Schistosomiasis

5. Obstructive uropathy

  • Calculus
  • Retroperitoneal fibrosis
  • Prostatic hypertrophy
  • Pelvic tumors

6. Systemic diseases

  • Diabetic nephropathy
  • Gout
  • Amyloidosis
  • Multiple myeloma
  • Radiation nephropathy

Chronic renal failure is due to progressive destruction of nephrons. As the nephrons are destroyed, the parenchyma shrinks and it is replaced by fibrosis. The remaining nephrons undergo hypertrophy. This gives an appearance of granular contracted kidney. But the renal functions are maintained by the hypertrophied nephrons. Since the concentrating function is impaired, Polyuria with urine of specific gravity around 1.010 (specific gravity of glomerular filtrate) occurs. Defective renal function leads to secondary hypertension, which in turn leads to deleterious influence on the kidney, brain, and heart. There is accumulation of phosphates, parathyroid hormone, urea, creatinine, guanidine, phenols and indoles in the body fluids.

Hypertension causes renal damage (in addition to being produced by It) and when it is severe, renal failure progress rapidly with the patient dying of uraemia or cardio vascular system complication, after a relatively short illness. If hypertension is absent or can be readily controlled, the patient may live for years, despite severe impairment of renal function. The early phase of the disease is asymptomatic, since the kidney has considerable reserve function. Symptoms and biochemical abnormalities are evident only when the renal function has deteriorated to less than 35% of the normal.

(In CRF the tubules loss their capacity to concentrate and dilute the urine, then the specific gravity become fixed at 1010.This       is called        isosthenuria). When the renal function is between 35 % and 25 % of the normal, symptoms like pallor, tiredness and nocturia are evident. Blood urea and serum creatinine are elevated. [Normal blood urea less than 40 mg/dl; creatinine— 0.4 to 1.4rng/dl] and serum bicarbonate may be decreased slightly [normal 24- 28 meq/lit]

Clinical   Feature:-
In the early stages of disease, the patient may be asymptomatic and the existence of renal insufficiency may be revealed by the discovery protenuria, anaemia, hypertension or raised blood urea during routine examination. When the renal function deteriorates slowly, patient remain asymptomatic until the glomerular filtration rate is 15m1/rnt or less.

Signs and symptoms of chronic renal failure referable to almost all system. They are as follows:-

1.Neurological: Fatigue, insomnia, reversal of sleep rhythm, peripheral neuropathy, muscular irritability, convulsion and coma. Low calcium level leads to increased neuro muscular irritability arid can leads to tetany and to convulsion. Loss of tendon jerk and slowing of nerve conduction velocities are also  present.

2.Gastro intestinal tract: Anorexia, nausea, vomiting and peptic ulcer. Nitrogenous waste product retension has an important effect on the gastrointestinal tract. Anorexia and vomiting tends to limit caloric intake leads to wasting. Constipation from reduced food intake. Some will develops ulceration at numerous points along the gastrointestinal tract with      profuse bloody      diarrhoea.

3.Hematological: Normochromic normocytic anaemia and bleeding tendencies due to platelet dysfunctions. A nitrogenous compound — guanidosuccinic acid contribute to platelet dysfunction. Patient with renal failure are usually uniformly anaemic even when they are maintained biochemically normal haemodialysis and when no bleeding tendency is apparent. It is thought that this anaemia is due to the lack of the hormone erythropoietin. Erythropoietin stimulate the erythropoisis. Erythropoietin is formed in the renal tissues probably due to the effect of Adrenal cortico trophic hormone.

4. Endocrine: Secondary hyperthyroidism, amenorrhea, infertility and impotence

5.Dermatological:Swallow pigmentation, intractable pruritus (calcium deposition in tissue especially in skin-giving rise to pruritus) excoriation and uremic frost (whitish precipitate of urea crystals on the skin occurring in advanced uremia) occur in skin. Normal urine contains a variety of pigments and has a yellowish brown appearance. In renal failure these pigments are retained in the body and imparting a bronzed appearance to the skin. Because of this bronzed appearance, most of the uraemic patients look less anaemic than they are.

6.Skeletal:Skeletal changes include mainly renal osteodystrophy, which includes osteomalacea, osteoporosis, ostitis fibrosa or rickets. Skeletal manifestations are due to disordered calcium and phosphate metabolism.

7.Cardio vascular system:Hypertension, cardiac failure, pericarditis, myocrdiopathy and accelerated atherosclerosis. Uraemic pericarditis was regarded as a harbinger of doom. Death was usual with in a few days of pericarditis being detected. The patient is usually complaints of left sided pleuritic pain and this pain has some postural characteristic. (For example: pain becomes less severe when the patient bends forward). Here there is a constant danger of bleeding in to the inflamed pericardial sac with cardiac temponade and sudden death. Diagnosis by X-ray and pericardial friction rub.

8.Occular: Red eye (due to conjuctival calcium deposition and congestion). Calcium deposition in the cornea and hypertensive retinopathy.

9.Respiratory: Kuss maul’s respiration, uremic lung (increased pulmonary capillary permeability and leading to transudation of fluid and radiological appearance similar to left        ventricular       failure) When the renal function falls below 5% of normal, the condition is termed “end stage renal failure.” The continued survival at this stage is possible only with renal transplantation. At present more than 50% of all cases of end stage renal failure are caused by diabetic nephropathy and hypertension.

Laboratory Studies

  • Serum electrolytes, BUN, and creatinine – The BUN and creatinine levels will be elevated in patients with chronic kidney disease. Hyperkalemia or low bicarbonate levels may be present in patients with chronic kidney disease.
  • Serum calcium, phosphate, vitamin D, and intact parathyroid hormone (PTH) levels are obtained to look for evidence of renal bone disease.
  • CBC count – Normochromic normocytic anemia is commonly seen in chronic kidney disease. Other underlying causes of anemia should be ruled out.
  • Serum albumin – Patients may have hypoalbuminemia due to urinary protein loss or malnutrition.
  • Lipid profile – A lipid profile should be performed in all patients with chronic kidney disease because of their increased risk of cardiovascular disease.
  • Urinalysis – Dipstick proteinuria may suggest a glomerular or tubulointerstitial problem. The urine sediment finding of RBCs, RBC casts, suggests proliferative glomerulonephritis. Pyuria and/or WBC casts are suggestive of interstitial nephritis (particularly if eosinophiluria is present) or urinary tract infection.
  • Spot urine collection for total protein-to-creatinine ratio allows reliable approximation (extrapolation) of total 24-hour urinary protein excretion. A value of greater than 2 g is considered to be within the glomerular range, and a value of greater than 3-3.5 g is within the nephrotic range; less than 2 is characteristic of tubulointerstitial problems.
  • Twenty-four–hour urine collection for total protein and CrCl
  • In certain cases, the following tests may be ordered as part of the evaluation of patients with chronic kidney disease:
    • Serum and urine protein electrophoresis to screen for a monoclonal protein possibly representing multiple myeloma
    • Antinuclear antibodies (ANA), double-stranded DNA antibody levels to screen for systemic lupus erythematosus
    • Serum complement levels – May be depressed with some glomerulonephritides
    • C-ANCA and P-ANCA levels – Helpful if positive in diagnosis of Wegener granulomatosis and polyarteritis nodosa or microscopic polyangiitis, respectively
    • Anti–glomerular basement membrane (anti-GBM) antibodies – Highly suggestive of underlying Goodpasture syndrome
    • Hepatitis B and C, HIV, Venereal Disease Research Laboratory (VDRL) serology – Conditions associated with some glomerulonephritides
  • Plain abdominal x-ray – Particularly useful to look for radio-opaque stones or nephrocalcinosis
  • Intravenous pyelogram – Not commonly used because of potential for intravenous contrast renal toxicity; often used to diagnose renal stones
  • Renal ultrasound – Small echogenic kidneys are observed in advanced renal failure. Kidneys usually are normal in size in advanced diabetic nephropathy, where affected kidneys initially are enlarged from hyperfiltration. Structural abnormalities, such as polycystic kidneys, also may be observed. This is a useful test to screen for hydronephrosis, which may not be observed in early obstruction, or involvement of the retroperitoneum with fibrosis, tumor, or diffuse adenopathy. Retrograde pyelogram may be indicated if a high index of clinical suspicion for obstruction exists despite a negative study finding.

Imaging Studies

  • Renal radionuclide scan – Useful to screen for renal artery stenosis when performed with captopril administration but is unreliable for GFR of less than 30 cc/min; also quantitates differential renal contribution to total GFR
  • CT scan – CT scan is useful to better define renal masses and cysts usually noted on ultrasound. Also, it is the most sensitive test for identifying renal stones. IV contrast-enhanced CT scans should be avoided in patients with renal impairment to avoid acute renal failure; this risk significantly increases in patients with moderate-to-severe chronic kidney disease. Dehydration also markedly increases this risk.
  • MRI is very useful in patients who require a CT scan but who cannot receive intravenous contrast. It is reliable in the diagnosis of renal vein thrombosis, as are CT scan and renal venography. Magnetic resonance angiography also is becoming more useful for diagnosis of renal artery stenosis, although renal arteriography remains the criterion standard.
  • Voiding cystourethrogram (VCUG) – Criterion standard for diagnosis of vesicoureteral reflux
  • The Cockcroft-Gault formula for estimating CrCl should be used routinely as a simple means to provide a reliable approximation of residual renal function in all patients with chronic kidney disease. The formulas are as follows:
    • CrCl (male) = ([140-age] X weight in kg)/(serum creatinine X 72)
    • CrCl (female) = CrCl (male) X 0.85
  • Alternatively, the Modification of Diet in Renal Disease (MDRD) Study equation could be used to calculate the GFR. This equation does not require a patient’s weight.3
  • Percutaneous renal biopsy is performed most often with ultrasound guidance and the use of a mechanical gun. It generally is indicated when renal impairment and/or proteinuria approaching the nephrotic range are present and the diagnosis is unclear after appropriate other workup. It is not indicated in the setting of small echogenic kidneys on ultrasound because these are severely scarred and represent chronic irreversible injury. The most common complication of this procedure is bleeding, which can be life threatening in a minority of occurrences.
  • Surgical open renal biopsy can be considered when the risk of renal bleeding is felt to be great, occasionally with solitary kidneys, or when percutaneous biopsy is technically difficult to perform.

Other Tests
The microscopic appearance of the “end stage kidney” is similar regardless of cause, which is why a biopsy in a patient with chronic renal failure yields little useful information. The cortex is fibrotic, the glomeruli are sclerotic, there are scattered chronic inflammatory cell infiltrates, and the arteries are thickened. Tubules are often dilated and filled with pink casts and give an appearance of “thyroidization.”

Histologic Findings
Renal histology in chronic kidney disease reveals findings compatible with the underlying primary renal diagnosis and, generally, findings of segmental and globally sclerosed glomeruli and tubulointerstitial atrophy, often with tubulointerstitial mononuclear infiltrates.


Self-Care at Home
Chronic kidney disease is a disease that must be managed in close consultation with your health care practitioner. Self-treatment is not appropriate.

  • There are, however, several important dietary rules you can follow to help slow the progression of your kidney disease and decrease the likelihood of complications.
  • This is a complex process and must be individualized, generally with the help of your health care practitioner and a registered dietitian.

The following are general dietary guidelines:

  • Protein restriction: Decreasing protein intake may slow the progression of chronic kidney disease. A dietitian can help you determine the appropriate amount of protein for you.
  • Salt restriction: Limit to 4-6 grams a day to avoid fluid retention and help control high blood pressure.
  • Fluid intake: Excessive water intake does not help prevent kidney disease. In fact, your doctor may recommend restriction of water intake.
  • Potassium restriction: This is necessary in advanced kidney disease because the kidneys are unable to remove potassium. High levels of potassium can cause abnormal heart rhythms. Examples of foods high in potassium include bananas, oranges, nuts, and potatoes.
  • Phosphorus restriction: Decreasing phosphorus intake is recommended to protect bones. Eggs, beans, cola drinks, and dairy products are examples of foods high in phosphorus.

Other important measures that you can take include:

  • carefully follow prescribed regimens to control your blood pressure and/or diabetes;
  • stop smoking; and
  • lose excess weight.

In chronic kidney disease, several medications can be toxic to the kidneys and may need to be avoided or given in adjusted doses. Among over-the-counter medications, the following need to be avoided or used with caution:

  • Certain analgesics: Aspirin; nonsteroidal antiinflammatory drugs (NSAIDs, such as ibuprofen [Motrin, for example])
  • Fleets or phosphosoda enemas because of their high content of phosphorus
  • Laxatives and antacids containing magnesium and aluminum such as magnesium hydroxide (Milk of Magnesia) and famotidine (Mylanta)
  • Ulcer medication H2-receptor antagonists: cimetidine (Tagamet), ranitidine (Zantac), (decreased dosage with kidney disease)
  • Decongestants such as pseudoephedrine (Sudafed) especially if you have high blood pressure
  • Alka Seltzer, since this contains large amounts of salt
  • Herbal medications

“If you have a condition such as diabetes, high blood pressure, or high cholesterol underlying your chronic kidney disease, take all medications as directed and see your health care practitioner as recommended for follow-up and monitoring”.

Medical Treatment

There is no cure for chronic kidney disease in allopathy. The four goals of therapy are to:

1.   slow the progression of disease;

2.   treat underlying causes and contributing factors;

3.   treat complications of disease; and

4.   replace lost kidney function.

Strategies for slowing progression and treating conditions underlying chronic kidney disease include the following:

  • Control of blood glucose: Maintaining good control of diabetes is critical. People with diabetes who do not control their blood glucose have a much higher risk of all complications of diabetes, including chronic kidney disease.
  • Control of high blood pressure: This also slows progression of chronic kidney disease. It is recommended to keep your blood pressure below 130/80 mm Hg if you have kidney disease. It is often useful to monitor blood pressure at home. Blood pressure medications known as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) have special benefit in protecting the kidneys.
  • Diet: Diet control is essential to slowing progression of chronic kidney disease and should be done in close consultation with your health care practitioner and a dietitian. For some general guidelines, see the Self-Care at Home section of this article.

The complications of chronic kidney disease may require medical treatment.

  • Fluid retention can be treated with any of a number of diuretic medications, which remove excess water from the body. However, these drugs are not suitable for all patients.
  • Anemia can be treated with erythropoiesis stimulating agents such as erythropoietin or darbepoetin (Aranesp, Aranesp Albumin Free, Aranesp SureClick). Erythropoiesis stimulating agents are a group of drugs that replace the deficiency of erythropoietin, which is normally produced by healthy kidneys. Often, patients treated with such drugs require iron supplements by mouth or sometimes even intravenously.

Bone disease develops in kidney disease due to an inability to excrete phosphorus and a failure to form activated Vitamin D. In such circumstances, your physician may prescribe drugs binding phosphorus in the gut, and may prescribe active forms of vitamin D.

  • Acidosis may develop with kidney disease. The acidosis may cause breakdown of proteins, inflammation, and bone disease. If the acidosis is significant, your doctor may use drugs such as sodium bicarbonate (baking soda) to correct the problem.

Renal Replacement Therapies
In end-stage kidney disease, kidney functions can be replaced only by dialysis or by kidney transplantation. The planning for dialysis and transplantation is usually started in Stage 4 of chronic kidney disease. Most patients are candidates for both hemodialysis and peritoneal dialysis (see below). There are few differences in outcomes between the two procedures. Your physician or an educator will discuss the appropriate options with you and help you make a decision that will match your personal and medical needs. It is best to choose your modality of dialysis after understanding both procedures and matching them to your lifestyle, daily activities, schedule, distance from the dialysis unit, support system, and personal preference.

Your doctor will consider multiple factors when recommending the appropriate point to start dialysis, including your laboratory work and your actual or estimated glomerular filtration rate, nutritional status, fluid volume status, the presence of symptoms compatible with advanced kidney failure, and risk of future complications. Dialysis is usually started before individuals are very symptomatic or at risk for life-threatening complications.

There are two types of dialysis 1) hemodialysis (in-center or home) and 2) peritoneal dialysis. Before dialysis can be initiated, a dialysis access has to be created. 

Dialysis Access

A vascular access is required for hemodialysis so that blood can be moved though the dialysis filter at rapid speeds to allow clearing of the wastes, toxins, and excess fluid. There are three different types of vascular accesses: arteriovenous fistula (AVF), arteriovenous graft, and central venous catheters.

1. Arteriovenous fistula (AVF): The preferred access for hemodialysis is an AVF, wherein an artery is directly joined to a vein. The vein takes two to four months to enlarge and mature before it can be used for dialysis. Once matured, two needles are placed into the vein for dialysis. One needle is used to draw blood and run through the dialysis machine. The second needle is to return the cleansed blood. AVFs are less likely to get infected or develop clots than any other types of dialysis access.

2. Arteriovenous graft: An arteriovenous graft is placed in those who have small veins or in whom a fistula has failed to develop. The graft is made of artificial material and the dialysis needles are inserted into the graft directly.

3. Central venous catheter: A catheter may be either temporary or permanent. These catheters are either placed in the neck or the groin into a large blood vessel. While these catheters provide an immediate access for dialysis, they are prone to infection and may also cause blood vessels to clot or narrow.

Peritoneal access (for peritoneal dialysis): A catheter is implanted into the abdominal cavity (lined by the peritoneum) by a minor surgical procedure. This catheter is a thin tube made of a soft flexible material, usually silicone or polyurethane. The catheter usually has one or two cuffs that help hold it in place. The tip of the catheter may be straight or coiled and has multiple holes to allow egress and return of fluid. Though the catheter can be used immediately after implantation, it is usually recommended to delay peritoneal dialysis for at least 2 weeks so as to allow healing and decrease the risk of developing leaks.


Hemodialysis involves circulation of blood through a filter or dialyzer on a dialysis machine.

  • The dialyzer has two fluid compartments and is configured with bundles of hollow fiber capillary tubes.
  • Blood in the first compartment is pumped along one side of a semipermeable membrane, while dialysate (the fluid that is used to cleanse the blood) is pumped along the other side, in a separate compartment, in the opposite direction.
  • Concentration gradients of substances between blood and dialysate lead to desired changes in the blood composition, such as a reduction in waste products (urea nitrogen and creatinine); a correction of acid levels; and equilibration of various mineral levels.
  • Excess water is also removed.
  • The blood is then returned to the body.

Hemodialysis may be done in a dialysis center or at home. In-center hemodialysis typically takes three to five hours and is performed three times a week. You will need to travel to a dialysis center for in-center hemodialysis.

Some centers may offer the option of nocturnal (night-time) hemodialysis wherein the therapy is delivered while you sleep. Long nocturnal dialysis offers patients a better survival and an improvement in their quality of life.

Home hemodialysis is possible in some situations. A care partner is needed to assist you with the dialysis treatments. A family member or close friend are the usual options, though occasionally people may hire a professional to assist with dialysis. Home hemodialysis may be performed as traditional three times a week treatments, long nocturnal (overnight) hemodialysis, or short daily hemodialysis. Daily hemodialysis and long nocturnal hemodialysis offer advantages in quality of life and better control of high blood pressure, anemia, and bone disease.

Peritoneal dialysis
Peritoneal dialysis utilizes the lining membrane (peritoneum) of the abdomen as a filter to clean blood and remove excess fluid. Peritoneal dialysis may be performed manually (continuous ambulatory peritoneal dialysis) or by using a machine to perform the dialysis at night (automated peritoneal dialysis).

  • About 2 to 3 liters of dialysis fluid are infused into the abdominal cavity through the access catheter. This fluid contains substances that pull wastes and excess water out of neighboring tissues.
  • The fluid is allowed to dwell for two to several hours before being drained, taking the unwanted wastes and water with it.
  • The fluid typically needs to be exchanged four to five times a day.
  • Peritoneal dialysis offers much more freedom compared to hemodialysis since patients do not need to come to a dialysis center for their treatment. You can carry out many of your usual activities while undergoing this treatment. This may be the preferable therapy for children.

Most patients are candidates for both hemodialysis and peritoneal dialysis. There are little differences in outcomes between the two procedures. Your physician may recommend one kind of dialysis over the other based on your medical and surgical history. It is best to choose your modality of dialysis after understanding both procedures and matching them to your lifestyle, daily activities, schedule, distance from the dialysis unit, support system, and personal preference.

Complication of dialysis:-

  • Nausea & vomiting
  • Hypotension

Kidney transplantation offers the best outcomes and the best quality of life. Successful kidney transplants occur every day in all over the world. Transplanted kidneys may come from living related donors, living unrelated donors, or people who have died of other causes (cadaveric donors). In people with type I diabetes, a combined kidney-pancreas transplant is often a better option.

However, not everyone is a candidate for a kidney transplant. People need to undergo extensive testing to ensure their suitability for transplantation. Also, there is a shortage of organs for transplantation, requiring waiting times of months to years before getting a transplant.

A person who needs a kidney transplant undergoes several tests to identify characteristics of his or her immune system. The recipient can accept only a kidney that comes from a donor who matches certain of his or her immunologic characteristics. The more similar the donor is in these characteristics, the greater the chance of long-term success of the transplant. Transplants from a living related donor generally have the best results.

Transplant surgery is a major procedure and generally requires four to seven days in the hospital. All transplant recipients require lifelong immunosuppressant medications to prevent their bodies from rejecting the new kidney. Immunosuppressant medications require careful monitoring of blood levels and increase the risk of infection as well as some types of cancer. 

Prognosis:-Many people are not diagnosed with chronic kidney disease until they have lost much of their kidney function.

There is no cure for chronic kidney disease. Untreated, it usually progresses to end-stage renal disease. Lifelong treatment may control the symptoms of chronic kidney disease.


  • Anemia
  • Bleeding from the stomach or intestines
  • Bone, joint, and muscle pain
  • Changes in blood sugar
  • Damage to nerves of the legs and arms (peripheral neuropathy)
  • Dementia
  • Fluid buildup around the lungs (pleural effusion)
  • Heart and blood vessel complications
    • Congestive heart failure
    • Coronary artery disease
    • High blood pressure
    • Pericarditis
    • Stroke
  • High phosphorous levels
  • High potassium levels
  • Hyperparathyroidism
  • Increased risk of infections
  • Liver damage or failure
  • Malnutrition
  • Miscarriages and infertility
  • Seizures
  • Weakening of the bones and increased risk of fractures 

PREVENTION:- Treating the condition that is causing the problem may help prevent or delay chronic kidney disease. People who have diabetes should control their blood sugar and blood pressure levels and should not smoke.  

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