Renal necrosis

Glomerulonephritis, pyelonephritis, renal infarction, papillary necrosis, renal tumors, kidney stones Pyelonephritis, interstitial nephritis... 

Acute exposure of rats to high concentrations (up to 40,000 ppm) has resulted in convulsions, pulmonary edema, respiratory arrest, and death. In rats repeatedly exposed at 600 ppm, death was attributed to renal papillary necrosis renal toxicity was not present in rabbits similarly exposed. Exposure of rabbits to 300 or 600 ppm resulted in convulsions and hyperactivity, moderate inflammation of nasal tissues, and some inflammation of the trachea or bronchi. Subchronic studies found that rats exposed at 3 00 ppm had mottled incisor teeth, minimal renal effects, pulmonary histiocytosis, inflammation of nasal tissues, and cerebral vacuolation. 

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... 

Noncardiac pulmonary edema Pulmonary necrosis Renal necrosis... 

Additional indications for GCs include certain types of shock, hepatic diseases (e.g., hepatic necrosis), renal diseases (e.g., idiopathic nephrotic syndrome), and certain respiratory disorders (e.g., pulmonary sarcoidosis). It should be understood that in many of the conditions GCs are palliative at best and that in some instances their use may be controversial. 

Urogenital System Nephritis Nephrosis Tubular necrosis Renal dysfunction Bladder dysfunction Nephrolythiasis... 

Intoxication by aflatoxkis is referred to as aflatoxicosis. Edema and necrosis of hepatic and renal tissues seem characteristic of aflatoxicosis, and hemorrhagic enteritis accompanied by nervous symptoms often appear ki experimental animals. The mode of action of aflatoxkis kivolve an kiteraction with DNA and inhibition of the polymerases responsible for DNA and RNA synthesis (96). 

A large and rapidly growing number of clinical trials (phase I and phase II) evaluating the potential of DNA vaccines to treat and prevent a variety of human diseases are currently being performed ( http // clinicaltrials.gov) however, there is yet no licensed DNA vaccine product available for use in humans. The clinical trials include the treatment of various types of cancers (e.g., melanoma, breast, renal, lymphoma, prostate, and pancreas) and also the prevention and therapy of infectious diseases (e.g., HIV/ABDS, malaria, Hepatitis B vims, Influenza vims, and Dengue vims). So far, no principally adverse effects have been reported from these trials. The main challenge for the development of DNA vaccines for use in humans is to improve the rather weak potency. DNA vaccines are already commercially available for veterinary medicine for prevention of West Nile Vims infections in horses and Infectious Hematopoetic Necrosis Vims in Salmon. 

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). 

Proximal tubule cells are exquisitely sensitive to vasculat disturbances and acute tubular necrosis (ATN) can occur naturally in areas of poor perfusion resulting from falling blood pressure, or vasospasm of renal vessels or arterioles. In other words hypoxia associated with partial ischaemia can cause severe damage. It is not then surprising that anoxia associated with iatrogenic, surgically induced total ischaemia produces irreversible damage within a short time unless steps are taken to prevent it. 

Loop diuretics (dose depends on severity of renal insufficiency) ° Not directly beneficial in established acute tubular necrosis. 

Patients at greatest risk for mortality from acute pancreatitis are those who have multi-organ failure (e.g., hypotension, respiratory failure, or renal failure), pancreatic necrosis, obesity, volume depletion, greater than 70 years of age, and an elevated APACHE II score.3,4 The Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II score is a rating scale of disease severity in critically ill patients. 

NSAIDs can cause renal insufficiency when administered to patients whose renal function depends on prostaglandins. Patients with chronic renal insufficiency or left ventricular dysfunction, the elderly, and those receiving diuretics or drugs that interfere with the renin-angiotensin system are particularly susceptible. Decreased glomerular filtration also may cause hyperkalemia. NSAIDs rarely cause tubulointerstitial nephropathy and renal papillary necrosis. 

Genitourinary Renal papillary necrosis, hematuria, hyposthenuria, proteinuria, nephritic syndrome, tubular dysfunction,... 

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. 

K14. Kohan, D. E., Role of endothelin and tumour necrosis factor in the renal response to sepsis. Nephrol. Dial. Transplant. 9-4,73-77 (1994). 

O. mykiss 5-80 Juveniles exposed for 28 days had alterations of renal corpuscles and renal tubules at 5, 10, 20, or 40 pg/L exposures necrosis of endothelial cells and renal hematopoietic tissue were prominent at 80 pg/L 17... 

The most common adverse effects involve the GI system (gastritis, bleeding, and perforation), kidneys (renal papillary necrosis, reduced creatinine clearance [CLcr]), cardiovascular system (sodium and fluid retention, increased blood pressure), and CNS (impaired cognitive function, headache, dizziness). 

IV colchicine should be avoided because it is associated with serious adverse effects (e.g., bone marrow suppression, tissue necrosis from local extravasation, disseminated intravascular coagulation, hepatocellular toxicity, and renal failure). If considered necessary, the recommended initial IV dose is 2 mg (if renal function is normal) diluted in 10 to 20 mL of normal saline administered slowly over 10 to 20 minutes in a secure, free-flowing IV line to avoid extravasation. This may be followed by two additional doses of 1 mg each at 6-hour intervals, with the total dose not exceeding 4 mg. After a full IV course, patients should not receive colchicine by any route for at least 7 days. 

Absolute contraindications to warfarin include active bleeding, hemorrhagic tendencies, pregnancy, and a history of warfarin-induced skin necrosis. It should be used with great caution in patients with a history of GI bleeding, recent neurosurgery, alcoholic liver disease, severe renal... 

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. 

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