Exceeds community acquired ARF by 5-10 times 35000 in79 to 650000 in2002, 13% /year
5-20% of critically ill people suffer from ARF
Factors that alter intrarenal hemodynamics, either by increasing afferent arteriolar constriction or by causing efferent arteriolar vasodilatation, may also play a significant role in the development of prerenal azotemia by decreasing glomerular capillary pressure.
The mean increase in serum creatinine in patients with CKD treated with ACEI or ARB is, however, less than 30%
There is no need to discontinue ACEI or ARB therapy in response to smaller increments in serum creatinine. Once reversible factors, such as volume depletion, have been treated and renal function has returned to baseline, therapy with ACEI or ARB can be cautiously reinstituted.
It was initially thought that the renal dysfunction resulted from increased renal parenchymal pressure; however, data now suggest that decreased perfusion associated with increased renal venous pressure is the primary mechanism of renal dysfunction
Postrenal acute renal failure is caused by the anatomic obstruction to the flow of urine. When urinary tract obstruction is unilateral and the contralateral kidney is normal, the plasma creatinine concentration is usually normal or only minimally elevated and clinical ARF does not develop. Renal failure becomes manifest when the obstruction is bilateral (or below the level of the bladder) or is unilateral with dysfunction or absence of the contralateral kidney.
Intrinsic processes that result in ARF are categorized according to the primary site of anatomic injury
2 ends of the spectrum of renal reponse to hypoperfusion
The initiation phase refers to that period during which patients are subject to factors known to cause ATN— e.g. , hypotension, ischemia, sepsis, and nephrotoxins—but have not yet developed overt parenchymal injury. It is during this period that ARF is potentially preventable. With the development of overt tubular injury, there is an abrupt fall in GFR and the clinical syndrome of ATN becomes manifest. During the maintenance phase, which typically lasts 1 to 2 wk but is highly variable and may be as short as a few days or as long as 4 to 6 wk, GFR remains markedly depressed. Urine volume during this phase is variable—although many patients are oliguric, patients may be non-oliguric with urine volumes greater than 400 to 500 ml/d. During the recovery phase, cellular regeneration and repair restore tubular integrity and GFR increases to normal or near normal values.
Muscle compression from immobilization as in drug induced coma
Obstruction with intratubular heme pigment casts. Proximal tubular cell injury mediated by free chelatable iron and by the heme center of myoglobin. Concurrent volume depletion and renal ischemia. With crush injury of muscle, for example,
urine alkalinization prevents heme-protein precipitation with Tamm-Horsfall protein, and therefore intratubular pigment cast formation. Alkalinization may also minimize the conversion of hemoglobin to the more toxic methemoglobin.
Picture on pathophysiology of HRS
As noted above, the rise in plasma creatinine with reductions in glomerular filtration rate may be minimized by the marked reduction in creatinine production. It is particularly important to exclude spontaneous bacterial peritonitis, which is complicated by acute renal failure that may be reversible in 30 to 40 percent of patients.