Acute renal failure manifestations/treatment

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. 

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. 

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. 

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. 

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...

A number of reports have appeared on the adverse effects of rifampicin on the kidney. Courtois and de Coninck reported a case of acute renal failure requiring several transfusions and multiple periods of haemodialysis. Nephrotoxicity in this case developed when rifampicin was re-introduced into the treatment schedule after a gap of several weeks (25 ). A similar case was reported by Hanzl et at. from Germany (26 ) and a further case in which the nephrotoxicity became manifest during a course of twice weekly therapy was described by Nessi et al. (27 ). These authors also reviewed the cases reported to date in the literature, showing that interruptions of treatment or treatment on an intermittent basis are a common feature to most of the reported cases. Eventual renal failure may or may not be preceded by a flu-like illness. Renal biopsy has been carried out in approximately a third of the reported cases and a picture of tubular interstitial necrosis has been seen. The results of immunological tests have not been consistent, and antibodies to rifampicin have not been demonstrated in every case. It is perhaps worthy of note that renal failure has only, so far, been reported in patients who have had a fairly long course of treatment. 

Hypermagnesemia occurs in acute or chronic renal failure, in hemodialysis, and in women receiving magnesium sulfate for treatment of preeclampsia. The clinical manifestations resemble the effects of curare. At serum Mg + levels of 2.5-5.0 mmol/L, cardiac conduction is affected, and at concentrations above 12.5 mmol/L, cardiac arrest occurs in diastole. Hypomagnesemia can occur in steatorrhea, alcoholism, diabetic ketoacidosis, and many other disorders. Tetany usually occurs at serum Mg " " concentrations below 1 mmol/L. 

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