Chronic renal failure

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Template:DiseaseDisorder infobox | }} Chronic renal failure (CRF, or "chronic kidney failure", CKF, or "chronic kidney disease", CKD) is a slowly progressive loss of renal function over a period of months or years and defined as an abnormally low glomerular filtration rate, which 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).

1 Signs and symptoms
2 Diagnosis
3 Causes
4 Treatment
5 References
6 External links

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Signs and symptoms

Initially it is without symptoms and can only be detected as an increase in serum creatinine. As the kidney function decreases:

Blood pressure is increased (hypertension)
Urea accumulates, leading to uremia (symptoms ranging from lethargy to pericarditis and encephalopathy)
Potassium accumulates in the blood (known as hyperkalemia with symptoms ranging from malaise to fatal cardiac arrhythmias)
Erythropoietin synthesis is decreased (leading to anemia causing fatigue)
fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema
Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency) and hyperparathyroidism - leads to renal osteodystrophy and vascular calcification

CRF patients suffer from accelerated atherosclerosis and have higher incidence of cardiovascular disease, with a poorer prognosis.

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Diagnosis

In many CRF patients, previous renal disease or other underlying diseases are already known. A small number presents with CRF of unknown cause. In these patients, a cause is occasionally identified retrospectively.

It is important to differentiate CRF from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys in CRF are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CRF and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible.

Numerous uremic toxins (see link) are accumulating in chronic renal failure patients treated with standard dialysis. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.

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Causes

The most common causes of CRF in North America and Europe are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.

Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as:

Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis
Glomerular, comprising a diverse group and subclassified into
- Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephritis
- Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis
Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
Obstructive such as with bilateral kidney stones and diseases of the prostate

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Treatment

The goal of therapy is to slow down or halt the otherwise relentless progression of CRF to ESRD. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression to ESRD.Template:Ref Template:Ref

Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary, as is calcium. Phosphate binders are used to control the serum phosphate levels, which are usually elevated in chronic renal failure.

After ESRD occurs, renal replacement therapy is required, in the form of either dialysis or a transplant.

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References

Template:Note Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454
Template:Note Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863

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