Acute renal failure manifestations

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

The pathophysiology, clinical manifestations, diagnosis, and treatment of acute renal failure and chronic kidney disease (CKD) or end-stage renal disease are discussed in Chaps. 75 and 76, respectively. 

Extrapyramidal symptoms (EPS) Dystonic reactions develop primarily with the use of traditional antipsychotics. EPS has occurred during the administration of haloperidol and pimozide frequently, often during the first few days of treatment. Neuroleptic malignant syndrome (NMS) A potentially fatal symptom complex sometimes referred to as NMS has been reported in association with administration of antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, cardiac dysrhythmia). Additional signs may include elevated creatine phosphokinase, rhabdomyolysis, and acute renal failure. 

Shin YM, Han HS, Goo JC, Park SS, Lim SW, Kim M-O, Kwon SK, Kim H-Y, Han GS (2005) Clinical manifestations of acute renal failure with loin pain developed after anaerobic exercise (in Korean with English abstract). Korean J Nephrol 24 64-70... 

Simvastatin, like other inhibitors of HMG-CoA reductase, occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase (CK) 10 times above the upper limit of normal (ULN). Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and very rare fatalities have occurred. 

The mechanism of BCNU-induced nephrotoxicity is most hkely based on a direct nephrotoxic effect but differs from that of streptozotocin manifested by proximal tubular dysfunction and acute renal failure that may abate when the drug is discontinued. 

Celiptinium is useful in the treatment of metastatic breast cancer and is useful in combination therapy because of minimal hematotoxicity. Acute and chronic renal failures have been detected in patients treated with celiptinium. Acute renal failure is dose dependent, while chronic effects appear to be cumulative in nature. The primary manifestation of celiptinium nephrotoxicity is tubular necrosis with celiptinium-induced lipid peroxidation in proximal tubular cells proposed as the mechanism of toxicity. 

Hypertension and tachycardia are the primary toxic manifestations of pseudoephedrine overdose. An amount of more than three or four times the maximum daily dosage for adults or children may produce symptoms of jS-adrenergic stimulation. In severe poisonings, cardiac dysrhythmias and cerebral hemorrhage due to hypertensive crisis may occur. Anxiety, muscle tremor, and seizures may result from CNS stimulation. Hallucinations, drowsiness, and/or irritability are more common symptoms exhibited by children. Hypokalemia and hyperglycemia may be noted. Acute renal failure and rhabdomyolysis have occurred in rare instances with large overdoses. 

In a clinical study, several patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure were treated with phenothiazine, butyrophenone (haloperidol), benzamide, iminomide, benzisox-azole, antidepressants and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia [ 184], The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever and excessive perspiration. All patients were successfully cured of acute renal failure by haemodialysis or haemodiafiltration. 

These acid metabolites are responsible for much of the toxicity of ethylene glycol, the clinical manifestations of which include neurological abnormalities (CNS depression in severe cases, coma and convulsions), severe metabolic acidosis, acute renal failure, and cardiopulmonary failure. The serum concentration of glycolic acid correlates more closely with clinical symptoms and mortality than does the concentration of ethylene glycol. Secause of the rapid elimination of ethylene glycol (ti/2 3 hours), its serum concentration may be low or undetectable at a time when that for glycolic acid remains elevated. Thus the determi-... 

Late complications of acute CN poisoning may include acute renal failure (Megarbane and Baud, 2003), rhabdomyolysis (Brivet et al., 1983), CNS degenerative changes and diffuse cerebral edema (Fligner et al., 1987 VameU et al., 1987), and neuropsychiattic manifestations including paranoid psychosis (Kales et al., 1997). 

Acute allergic interstitial nephritis is the underlying cause for up to 3% of all cases of acute renal failure. Clinical manifestations of AIN typically present about 14 days after initiation of therapy and include fever, maculopapular rash, eosinophilia, pyuria, hematuria, proteinuria, and oliguria. 

Renal Effects. Blood and urine analyses of workers exposed to RDX in the air for acute (Kaplan et al. 1965) or chronic durations (Hathaway and Buck 1977) did not reveal any kidney toxicity. Although no renal toxicity was observed after exposure to RDX dust, there were some manifestations of renal damage after possible inhalation exposure to C-4 (91 % RDX) transient oliguria and proteinuria in two patients and acute renal failure in one case (Ketel and Hughes 1972). 

Tacrolimus acute nephrotoxicity can manifest itself as clinically significant acute renal failure, asymptomatic changes in glomerular filtration rate [254,527-533] or hemolytic-uremic syndrome [534-538]. Even being a cause of hemolytic-uremic syndrome, tacrolimus has been advocated as an alternative treatment for patients with CsA-induced hemolytic-uremic syndrome [539, 540]. However, cases of patients with CsA-induced hemolytic-uremic syndrome that recurred after conversion from CsA to tacrolimus have been reported, indicating that this approach is not completely safe [541]. 

Acute renal failure or deterioration has frequently been cited in association with IFN-a treatment of Hepatitis C and even Hepatitis B. It is well known that Hepatitis C virus infection causes glomerulonephritis (GN). Membranoproliferative GN is the most common manifestation and biopsy specimens have shown deposition of immune complexes composed of HCV related antigen and cryoglobulin. The difficulty lies in distinguishing glomerulonephritis caused by Hepatitis C from glomerulonephritis seen in association with IFN-a therapy or from occult underlying renal disease that is exacerbated by IFN-a. 

A. After an acute overdose, symptoms are typically delayed for 2-12 hours and include nausea, vomiting, abdominal pain, and severe bloody diarrhea. Shook results from depressed cardiac contractility and fluid loss into the gastrointestinal tract and other tissues. Delirium, seizures, or coma may occur. Lactic acidosis related to shock and inhibition of cellular metabolism is common. Other manifestations of acute colchicine poisoning include acute myocardial injury, rhabdomyolysis with myoglobinuria, disseminated intravascular coagulation, and acute renal failure. 

D. Systemic manifestations of intoxication include CNS depression, delirium, seizures, and metabolic acidosis. Skeletal muscle necrosis, acute renal failure, and hepatic necrosis have also been reported in fatal cases. 

PTH is known to have central nervous system effects in humans even in the absence of impaired renal function. Neuropsychiatric symptoms have been reported to be among the most common manifestations of primary hyperparathyroidism (Heath et al., 1980 Luxenberg et al., 1984). Patients with primary hyperparathyroidism also have EEG changes similar to those observed in patients with acute renal failure (Cooper etal., 1978 Goldstein Massry, 1980). The common denominator appears to be elevated plasma levels of PTH (Cogan et al., 1978 Cooper et al., 1978 Guisado et al., 1975 Mahoney Arieff, 1982). 

Renal failure can be acute— rapid loss of renal function owing to kidney damage from such conditions as prolonged hypotension or hypovolemia or owing to nephrotoxic drugs. The key manifestations of acute renal failure (ARF) are... 

At various stages of renal failure, imbalances in fluids, electrolytes, and acid-base status are noted. In acute renal failure, symptoms may occur suddenly, last for a period of time, and then resolve with treatment (although some residual loss of function may remain). However, in chronic renal failure, imbalances are ongoing and require regular treatment to maintain stability. The manifestations of renal failure are similar, whether acute or chronic, depending on the underlying cause, but chronic renal failure evidences a progressive loss of renal cells that affects several body functions. 

The primary manifestations of renal failure and usual treatments are fisted in Table 11-1. While treatment of acute renal failure centers on eliminating the underlying cause, managing symptoms, and preventing complications, the care provided in both acute and chroific renal failure is similar for the body systems affected. 

Table 11-1 Primary Manifestations of Acute Renal Failure and Recommended Treatment Regimens...

Adverse reactions to rifamycins suggested to be immune mediated include a flu -like syndrome, acute renal failure, hemolytic anemia, and thrombocytopenia. Other more typical manifestations of hypersensitivity include urticaria, contact dermatitis, erythema multiforme, vasculitis, and rarely Stevens-Johnson syndrome and toxic... 

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