Kidney failure may be due to acute injury or may develop as a result of slow progression. Chronic kidney disease occurs most frequently in those older than 65 years, often caused by diabetes and hypertension. Treatment of both acute and chronic conditions requires addressing the underlying condition, and carefully managing the water and electrolyte balance and other conditions resulting from the declining kidney function. Dialysis and kidney transplantation may be necessary.
Kidney failure is a severe deterioration of kidney function. Two principal classes of this condition are distinguished: acute and chronic kidney failure. However, some aspects of the pathophysiology are similar in acute kidney injury (AKI) and chronic kidney disease (CKD). For example, both can lead to end-stage kidney disease owing to the compensatory mechanisms of the kidney driving hypertrophy and hyperfiltration, which cause further injury in the residual nephrons .
Acute kidney failure (acute kidney injury, AKI) is due to a sudden injury, whereas chronic failure develops over a time scale of months, although AKI may contribute to the development of advanced chronic disease . Classification of AKI is either by the rate of increase in serum creatinine or by the decrease in urine volume . Acute failure can be classified as prerenal, intrinsic, and postrenal, depending on the site of the original lesion. Volume contraction (due to hemorrhage or other fluid loss) is a principal prerenal cause of decreased renal blood flow. Trauma to the kidneys can happen in the glomerular or tubular regions and may be due to hypoxia, drugs, or other reasons. Postrenal causes are attributable to downstream obstruction occurring in the ureter, bladder or urethra. About 1% of hospitalized patients undergoing general surgery will develop AKI . Several conditions, the most important ones in the USA being diabetes and hypertension, are associated with or cause chronic kidney disease. The incidence of CKD is rapidly rising in the above 65-year-old age group, at least partially owing to the increase in the metabolic syndrome. The worldwide prevalence of CKD is a little over 10% . Some hereditary conditions will result in CKD. Variants of proteins (such as apolipoprotein L1) and several polymorphisms have been found associated with increased incidence of CKD .
Patients with acute kidney injury complain of nausea and vomiting; they may be confused or have seizures in advanced stages. Oliguria is characteristic but not always present. Water and electrolyte level disturbances lead to fluid buildup. Dyspnea may result from fluid accumulation in the lungs, and chest pain may be present in cases of uremic pericarditis. The symptoms of the chronic disease are not unlike those occurring in AKI but develop more slowly. In the chronic disease (CKD), five stages are distinguished according to glomerular filtration rates (GFR), but in the initial stages, the GFR may be within normal limits. In the latter case, other markers (albuminuria, electrolyte disturbances) may be useful for classification. Symptoms are often lacking at the start of the disease (stages 1-3), but weight loss, tiredness, nocturia, and pruritus for extended times (months) may indicate CKD. In stage 4, when the GFR is less than a third of normal, signs of diminished kidney function are observed: hyperkalemia, hyperphosphatemia, peripheral and pulmonary edema indicate impaired electrolyte balance; anemia implies a decline in erythropoietin production; bone disease may, at least in part, be a consequence of hyperphosphatemia and acidosis; anorexia, nausea, encephalopathy, neuropathy, and seizures point to uremia. Other manifestations include cardiac and gastrointestinal problems.
A careful history is essential for the identification of the underlying disease. For the diagnosis of AKI, it is vital to review drug use and exposure to possible nephrotoxic substances (diagnostic contrast material), as well as events leading to loss of fluids. The most important elements of workup are serum (electrolytes, blood urea nitrogen, i.e., BUN, creatinine, and phosphate) and urine analysis, complete blood count, imaging, and renal biopsy.
When suspicion of impaired kidney function arises, often because of an incidental finding of high serum creatinine, the chronic or acute nature of the condition needs to be clarified. Observations that indicate AKI are daily increases in creatinine or BUN concentrations, oliguria, and relatively large kidneys detected on sonograms. Conversely, sonograms displaying small kidneys, chronic manifestations such as anemia, fatigue, nausea, and pruritus, and decreased estimated GFR indicate CKD. The tests can also show the source of the damage. A very high BUN to creatinine ratio suggests prerenal causes of AKI. If the urine does not become concentrated in the presence of volume contraction (indicated by oliguria), it points to an intrinsic kidney defect in AKI. Misshapen red blood cells in the urine point to glomerular injury (glomerulonephritis), whereas urine sediment that contains tubular cells reveals tubular damage. Ultrasonography helps in identifying obstructive pathologies. Additional tests may be carried out for specific diseases that are frequently associated with or known to cause kidney failure. The furosemide stress test, if it demonstrates the inability of the kidney to respond to the diuretic, can predict the progression of the acute disease .
New biomarkers for kidney function are being sought and found: cystatin C may have a role as a marker for glomerular filtration, and urinary neutrophil gelatinase-associated lipocalin as a predictor of AKI progression . Ultrasonography can be used to determine the size of the kidney, to detect renal disease, and to locate the sites of obstruction. Renal biopsy may be performed in some cases.