(Answered Case study) Mr. J.R. Is A 73-Year-Old Man, Who Was Admitted To The Hospital With Clinical Manifestations Of Gastroenteritis And Possible Renal Injury.

The diagnostic evaluation can be used to classify acute kidney injury as prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to identify the use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function. Physical examination should assess intravascular volume status and identify skin rashes indicative of systemic illness. The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in most patients, particularly in older men, to rule out obstruction. Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early diagnosis, and aggressive management are critical for improving outcomes. Causes of Acute Kidney Injury Prerenal Intrarenal vasoconstriction (hemodynamically mediated) Medications: nonsteroidal anti-inflammatory drugs,* angiotensin-converting enzyme inhibitors,* angiotensin receptor blockers,* cyclosporine (Sandimmune), tacrolimus (Prograf) Cardiorenal syndrome* Hepatorenal syndrome Abdominal compartment syndrome Hypercalcemia Systemic vasodilation (e.g., sepsis,* neurogenic shock) Volume depletion Renal loss from diuretic overuse,* osmotic diuresis (e.g., diabetic ketoacidosis*) Extrarenal loss from vomiting, diarrhea,* burns, sweating, blood loss Intrinsic renal Glomerular (e.g., postinfectious and other glomerulonephritis) Interstitial Medications: penicillin analogues,* cephalosporins,* sulfonamides, ciprofloxacin (Cipro), acyclovir (Zovirax), rifampin, phenytoin (Dilantin), interferon, proton pump inhibitors, nonsteroidal anti-inflammatory drugs Infections (e.g., direct infection of renal parenchyma or associated with systemic infections) Viruses: Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus Bacteria: Streptococcus species, Legionella species Fungi: candidiasis, histoplasmosis Systemic disease: sarcoidosis, lupus Tubular Ischemic: prolonged hypotension* Nephrotoxic: exogenous toxins (e.g., radiographic contrast agents,* aminoglycosides,* cisplatin, methotrexate, ethylene glycol, amphotericin B) and endogenous toxins (e.g., hemolysis and rhabdomyolysis [pigment nephropathy], tumor lysis syndrome, myeloma) Vascular Renal vein thrombosis, malignant hypertension, scleroderma renal crisis, renal atheroembolic disease,* and renal infarction Postrenal Extrarenal obstruction: prostate hypertrophy*; neurogenic bladder; retroperitoneal fibrosis; bladder, prostate, or cervical cancer Intrarenal obstruction: stones,* crystals (acyclovir, indinavir [Crixivan]), clots, tumors PRERENAL CAUSES Approximately 70 percent of community-acquired cases of acute kidney injury are attributed to prerenal causes. In these cases, underlying kidney function may be normal, but decreased renal perfusion associated with intravascular volume depletion (e.g., from vomiting or diarrhea) or decreased arterial pressure (e.g., from heart failure or sepsis) results in a reduced glomerular filtration rate. Autoregulatory mechanisms often can compensate for some degree of reduced renal perfusion in an attempt to maintain the glomerular filtration rate. In patients with preexisting chronic kidney disease, however, these mechanisms are impaired, and the susceptibility to develop acute-on-chronic renal failure is higher. Several medications can cause prerenal acute kidney injury. Notably, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular pressure. Nonsteroidal anti-inflammatory drugs also can decrease the glomerular filtration rate by changing the balance of vasodilatory/vasoconstrictive agents in the renal microcirculation. These drugs and others limit the normal homeostatic responses to volume depletion and can be associated with a decline in renal function. In patients with prerenal acute kidney injury, kidney function typically returns to baseline after adequate volume status is established, the underlying cause is treated, or the offending drug is discontinued. INTRINSIC RENAL CAUSES Intrinsic renal causes are also important sources of acute kidney injury and can be categorized by the component of the kidney that is primarily affected (i.e., tubular, glomerular, interstitial, or vascular). Acute tubular necrosis is the most common type of intrinsic acute kidney injury in hospitalized patients. The cause is usually ischemic (from prolonged hypotension) or nephrotoxic (from an agent that is toxic to the tubular cells). In contrast to a prerenal etiology, acute kidney injury caused by acute tubular necrosis does not improve with adequate repletion of intravascular volume and blood flow to the kidneys. Glomerular causes of acute kidney injury are the result of acute inflammation of blood vessels and glomeruli. Glomerulonephritis is usually a manifestation of a systemic illness (e.g., systemic lupus erythematosus) or pulmonary renal syndromes (e.g., Goodpasture syndrome, Wegener granulomatosis). Acute interstitial nephritis can be secondary to many conditions, but most cases are related to medication use, making patient history the key to diagnosis. In about one-third of cases, there is a history of maculopapular erythematous rash, fever, arthralgias, or a combination of these symptoms. POSTRENAL CAUSES Postrenal causes typically result from obstruction of urinary flow, and prostatic hypertrophy is the most common cause of obstruction in older men. Prompt diagnosis followed by early relief of obstruction is associated with improvement in renal function in most patients.