Kidneys acute renal failure

Renal Effects. Hemorrhage of the medullary layer of the kidneys was reported in three persons who died following ingeshon of endosulfan (Terziev et al. 1974). Acute renal failure was a major contributor to the deaths of two individuals who ingested unknown amounts of endosulfan (Blanco-Coronado et al. 1992 Loetal. 1995). In both cases, postmortem examination revealed extensive tubular necrosis. In contrast, no kidney lesions were found in a man who died 4 days after ingesting approximately 260 mg endosulfan/kg (Boereboom et al. 1998). 

O Equations to estimate creatinine clearance that incorporate a single creatinine concentration (e.g., Cockcroft-Gault) may underestimate or overestimate kidney function depending on whether acute renal failure is worsening or resolving. 

Tonelli M, Manns B, Feller-Kopman D. Acute renal failure in the intensive care unit a systematic review of the impact of dialytic modality on mortality and renal recovery. Am J Kidney Dis 2002 40 875-885. 

Acute renal failure Sudden loss of the kidney s ability to excrete wastes, concentrate urine, and remove electrolytes. 

Acute tubular necrosis A form of acute renal failure that results from toxic or ischemic (insufficient oxygen) injury to the cells in the proximal tubule of the kidney. 

Arsine affects the ability of the blood system to carry oxygen by destroying red blood cells. The lack of oxygen rapidly affects all body tissues, especially the central nervous system. Arsine may also affect the kidneys, liver, and heart. Most deaths related to arsine exposure are believed to be secondary to acute renal failure. Arsine is carcinogenic. 

Acute renal failure is a rare but serious side effect of ACE inhibitors preexisting kidney disease increases the risk. Bilateral renal artery stenosis or unilateral stenosis of a solitary functioning kidney renders patients dependent on the vasoconstrictive effect of angiotensin II on efferent arterioles, making these patients particularly susceptible to acute renal failure. 

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. 

Noiri et al. used AS-ODN to inhibit production of inducible nitric oxide synthase (INOS) in an attempt to prevent NO production in an ischaemic kidney. A single intravenous injection of iNOS AS-ODN attenuated acute renal failure and reduced the morphological abnormalities [129],... 

Renal dysfunctions can be diagnosed by different methods, depending on the severity of the condition. Examination of urine, which is produced by the kidneys, provides an important indication of renal insufficiency. The urine output, color, odor, acidity, specific gravity, and constituents are important prognostic factors of kidney status. However, in critically ill patients and in acute renal failures induced by several diseases including multiple organ failures and diabetes, urine examination may be impractical and redundant. Such patients require reliable and simple methods to diagnose the onset of renal failure. 

Concomitant use with sympathomimetic drugs, p-adrenoceptor antagonists, calcium channel-entry blockers and other cardioactive drugs may result in bradyarrhythmias, bigemini, or tachyarrhythmias. Cardiac rhythm should be closely monitored and drug dosages carefully adjusted. Digoxin is mainly excreted by the kidneys and plasma levels should be closely monitored in patients with acute renal failure and in those whose renal function is compromised. 

Severe hypotension can occur after initial doses of any ACE inhibitor in patients who are hypovolemic as a result of diuretics, salt restriction, or gastrointestinal fluid loss. Other adverse effects common to all ACE inhibitors include acute renal failure (particularly in patients with bilateral renal artery stenosis or stenosis of the renal artery of a solitary kidney), hyperkalemia, dry cough sometimes accompanied by wheezing, and angioedema. Hyperkalemia is more likely to occur in patients with renal insufficiency or diabetes. Bradykinin and substance P seem to be responsible for the cough and angioedema seen with ACE inhibition. 

Gastrointestinal complaints (eg, nausea, diarrhea, vomiting, flatulence) are the most common adverse effects but rarely require discontinuation of therapy. Other potential adverse effects include headache and asthenia. Tenofbvir-associated proximal renal tubulopathy causes excessive renal phosphate and calcium losses and 1-hydroxylation defects of vitamin D, and preclinical studies in several animal species have demonstrated bone toxicity (eg, osteomalacia). Monitoring of bone mineral density should be considered with long-term use in those with risk factors for or with known osteoporosis, as well as in children. Reduction of renal function over time, as well as cases of acute renal failure and Fanconi s syndrome, have been reported in patients receiving tenofovir alone or in combination with emtricitabine. For this reason, tenofovir should be used with caution in patients at risk for renal dysfunction. Tenofovir may compete with other drugs that are actively secreted by the kidneys, such as cidofovir, acyclovir, and ganciclovir. 

---