Chronic renal failure overview
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Chronic renal failure (CRF), also known as chronic kidney failure (CKF) or chronic kidney disease (CKD), or chronic renal insufficiency (CRI) is a slowly progressive loss of renal function over a period of months or years defined as an abnormally low glomerular filtration rate. The glomerular filtration rate is usually determined indirectly by the creatinine level in blood serum.
CRF that leads to severe illness and requires some form of renal replacement therapy (such as dialysis) is called end-stage renal disease (ESRD).
- CKD is defined as:
- Presence of markers of kidney damage for > 3 months, and may include abnormalities in markers in blood or urine, and imaging tests.
- GFR < 60 mL/min/1.73 m2 for > 3 months with or without other signs of kidney damage.
CRF begins with damage to the nephrons, the filtering units of the kidneys, due to diseases such as diabetes, hypertension, immune complex deposition, toxin exposure, and inflammation. To compensate for the decreased glomerular filtration rate by the damaged nephrons, healthy nephrons hypertrophy and start hyperfiltrating due to signals from the body. As the disease process progresses, this adaptive response becomes maladaptive, and the increased filtration pressure in the healthy nephrons leads to the distortion of its structural architecture, causing sclerosis and eventual dropout of these nephrons.
Epidemiology and Demographics
The incidence and prevalence of chronic renal failure varies enormously depending on the level of affluence of the country. Developed countries have higher incident rates of treated end-stage renal failure, whereas emerging countries have very low incident rates. People with disorders that have adverse effects on the kidneys such as diabetes, and hypertension have increased chances of developing CRF.
Disorders or habits that damage small blood vessels or the nephrons are risk factors for developing chronic renal failure. Some of the factors associated with CRF include diabetes, hypertension, autoimmune diseases, obesity, smoking, high cholesterol, heart disease, and racial background.
CRF is associated with diseases such as diabetic nephropathy, hypertension, glomerulonephritis, ischemic nephropathy, vasculitis, Hemolytic-uremic syndrome, IgA nephropathy, and polycystic kidney disease to name a few. Diseases of the blood vessels or diseases that damage the nephrons are usually linked to the development of CRF.
Differentiating Chronic renal failure from other Conditions
CRF can be discerned from acute renal failure by looking at the timeline of the rise of serum creatinine levels. Acute renal failure is identified by sharp rises in the levels of creatinine, while CRF is identified by a slow and gradual increase in serum creatinine.
Natural History, Complications and Prognosis
Repeated episodes of acute renal injury from infections, drugs, toxins and immunological damage may accelerate the progression to chronic renal failure, especially in the elderly. Once CRF is developed, the condition can cause systemic problems such as infertility, myopathy, sleep disorders, pruritis, congestive heart failure, and pulmonary edema amongst other problems. The prognosis and quality of life for a patient with CRF is poor. Data indicates that the overall death rate increases as kidney function decreases.
Chronic renal failure causes disturbances not only in the filtration function of the kidney, but also in the normal functioning of virtually every organ in the body. Symptoms and overt signs of kidney disease are often subtle or are absent until renal failure ensues. Thus, the diagnosis of chronic renal failure often takes the patient by surprise and may cause denial.
The kidneys play an important role in the regulation of serum concentration of sodium, potassium, calcium, phosphate, bicarbonate and chloride as well as levels of hemoglobin, hematocrit, blood pressure and extracellular volume. Hence, chronic injury to the kidneys can lead to abnormalities in the stable values of the above mentioned parameters.
Treatment is aimed at specific causes of chronic renal failure. It includes optimized glucose levels in patients with diabetes, management of blood pressure, immunomodulators for glomerulonephritis, emerging specific therapies to retard cytogenesis in polycystic kidney disease and replacement of critical hormones and chemicals produced and utilized by normally healthy kidneys. Any acceleration in the disease process should prompt a search for superimposed acute or subacute disease process that is potentially reversible. These include extravascular fluid volume depletion, urinary tract infection, obstructive uropathy, exposure to nephrotoxic agents such as NSAIDs or radiocontrasts, re-activation and flare of the primary disease like SLE or vasculitis.