Renal failure prerenal

Monitoring changes in UOP can help diagnose the cause of ARF. Acute anuria (less than 50 mL urine/day) is secondary to complete urinary obstruction or a catastrophic event (e.g., shock). Oliguria (400 to 500 mL urine/day) suggests prerenal azotemia. Nonoliguric renal failure (more... 

Common laboratory tests are used to classify the cause of ARF. Functional ARF, which is not included in this table, would have laboratory values similar to those seen in prerenal azotemia. However, the urine osmolality-to-plasma osmolality ratios may not exceed 1.5, depending on the circulating levels of antidiuretic hormone. The laboratory results listed under acute intrinsic renal failure are those seen in acute tubular necrosis, the most common cause of acute intrinsic renal failure. 

Acute renal failure due to NSAIDs is usually due to prerenal causes but may be caused by acute interstitial nephritis. Usually the worsening in renal function does not depend on dose (Muhlberg and Platt 1999). Use of NSAID is thus risky and may affect the elimination of concomitant medications. 

Renal damage is the most significant toxic reaction. Renal impairment occurs in nearly all patients treated with clinically significant doses of amphotericin. The degree of azotemia is variable and often stabilizes during therapy, but can be serious enough to necessitate dialysis. A reversible component is associated with decreased renal perfusion and represents a form of prerenal renal failure. An irreversible component results from renal tubular injury and subsequent dysfunction. 

Patients with nephrotic syndrome can develop acute renal failure as a consequence of intravascular hypovolemia and/or sepsis with subsequent prerenal azotemia or acute tubular necrosis. Renal hypoperfusion in these patients can be potentiated by the administration of diuretics, inhibitors of angiotensin-converting... 

Criteria Hepato- renal syn- drome Acute kidney failure Prerenal kidney insuf- ficiency... 

Renal failure In about 50% of patients with acute hver failure, renal insufficiency develops. This can be expressed in three forms (7.) prerenal kidney failure due to hypovolaemia, (2.) acute tubular necrosis, mainly secondary as a result of circulatory hypotension with cylindruria, a higher concentration of sodimn in the urine (50—70 mmol/1) and a reduced urine creatinine/ser m creatinine quotient (<20) or urine urea/serrrm urea quotient (<3), or (3.) hepatorenal syndrome. (41) (s. tab. 17.3)... 

A 43-year-old woman with rheumatoid arthritis developed dizziness having taken celecoxib 200 mg/day for 2 weeks. At the start of treatment she had normal renal function (104). Her serum creatinine was 670 pmol/l (7.4 mg/dl) and blood urea nitrogen 30 mmol/1 (90 mg/dl). Creatinine clearance was 16 ml/minute. Urinalysis was normal and casts were not present. Urinary chemical analysis showed a sodium concentration of 18 mmol/1, a fractional excretion of sodium of 0.3, and a renal failure index of 0.493, consistent with prerenal acute renal insufficiency. Celecoxib was withdrawn. Although her renal function then improved, her serum creatinine was still abnormal (4.7 mg/dl) 1 month later. 

Dopamine Prerenal renal failure cardiogenic shock 1-5 n,g/kg/min i.v. or 15 p.g/kg/min in severe hypotension... 

Dopamine p adrenergic ionotropic doperminergic vasodilatation a adrenergic vasoconstriction (high dose) and chronotropic effects Prerenal renal failure cardiogenic shock Decrease peripheral perfusion at high doses tachycardia increase myocardial oxygen demand... 

Prerenal renal failure Systemic hypoperfusion Intravascular volume depletion Dehydration Hemorrhage CHF Liver disease Nephrotic syndrome Overdiuresis... 

Laboratory Test Prerenal Azotemia Acute Intrinsic Renal Failure Postrenal Obstruction... 

Prerenal ARF—Acute renal failure caused by a reduction of renal blood flow. Often associated with volume depletion or poor cardiac function. 

Nephrotoxins or ischemic disorders can initiate acute renal failure. Shock, hemorrhage, septicemia, or vasodilation due to hypertensive medication can precipitate ischemic acute renal failure. Systemic reactions to certain drugs and nephrotoxins such as aminoglycoside antibiotics and heavy metals lead to acute renal failure. The extent of retention of creatinine and urea in blood is directly related to the severity of acute renal failure. This condition is not readily reversible and, as such, should be distinguished from reversible phenomena such as prerenal or postrenal azotemia, in which there is also an increase in levels of plasma urea and creatinine (13). In volume-depleted states, for example, diarrhea, the kidney is hypoprefused. This results in increased back diffusion of urea into the circulation from the tubular fluid because of the reduced urine flow. In addition to an increase in urea levels in circulation, there is also a slow increase in creatinine levels. Plasma urea and creatinine levels can be restored to normal within 24 hours by appropriate fluid and electrolyte replacement in prerenal azotemia. In condi-... 

Patients with prerenal azotemia have urinary sodium levels of less than 20 mEq/liter, consistent with normal tubular function. In contrast, patients with either acute renal failure or postrenal azotemia have urinary sodium levels greater than... 

Studies of the pathophysiology of acute renal failure has classically considered both tubular and vascular mechanisms [227,228]. In vitro techniques isolating either the vascular or tubular components have been developed. For example, the use of isolated proximal tubules in suspension or in culture allows the study of tubular mechanisms of injury in the absence of vascular factors [229] [230]. There are both in vitro and in vivo models to study vascular injury in the kidney. In vitro models include the study of vascular smooth muscle cells or endothelial cells in culture. In this section, the in vivo methods to evaluate the renal micro-circulation will be discussed. This is of relevance as many nephrotoxins exert their deleterious effects through pharmacologic actions on the resistance vasculature with parenchymal injury occurring as a consequence of ischemia. In clinical practice nephrotoxins may cause prerenal azotemia as a result of increased renal vascular resistance. Nephrotoxins that cause acute renal failure on a vascular basis include prostaglandin inhibitors e.g. aspirin, non-steroidal anti-... 

Renal failure can result from a variety of pathologic conditions. If renal impairment is rapid in onset and short in duration, then renal failure is described as acute. The primary cause of acute renal failure may be prerenal (i.e., acute congestive heart failure or shock), intrarenal (i.e., acute tubule necrosis) or postrenal (i.e., hypercalcemia). The condition generally is reversible however, complete restoration of renal function may take 6 to 12 months. 

Calculation of fractional excretion (FE) makes it possible to study certain tubular functions. Fractional means relative to creatinine. Most frequently, the FE of sodium (FEj j,) is calculated. For calculation, simultaneous determination of creatinine and of sodium in the serum and in spot urine is needed. FE a is helpful to distinguish prerenal failure from intrinsic renal failure. 

There are also drugs which by themselves can cause kidney failure. The mechanisms behind drugs negative effects on the kidneys are multiple. Among the most important is diminished blood flow to the kidneys (prerenal failure). Others are immunological damages to the nephrons caused by deposition of autoimmune complexes or direct nephrotoxicity caused by for example, antibiotics. The kidney function can also be damaged by post-renal obstructions, for example, kidney stones, urethral strictures or prostate hyperplasia (Ashley 2004). 

Acute renal insufficiency with or without oliguria can occur, usually in association with severe volume depletion in, which case renal function is rapidly restored with appropriate fluid therapy. The picture may resemble that of acute tubular necrosis but prerenal failure seems more likely. Histological biopsy findings show remarkably few abnormalities. 

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