Permanent renal damage

Acute drug-related hypersensitivity reactions (allergic responses) may cause tubulointerstitial nephritis, which will damage the tubules and interstitium. These reactions are most commonly observed with administration of methicillin and other synthetic antibiotics as well as furosemide and the thiazide diuretics. The onset of symptoms occurs in about 15 days. Symptoms include fever, eosinophilia, hematuria (blood in the urine), and proteinuria (proteins in the urine). Signs and symptoms of acute renal failure develop in about 50% of the cases. Discontinued use of the drug usually results in complete recovery however, some patients, especially the elderly, may experience permanent renal damage. 

Sirohmus is used for the prophylaxis of organ transplant rejection in combination with a calcineurin inhibitor and glucocorticoid. In patients at high risk for nephrotoxicity it has been combined with glucocorticoids and mycophenolate to avoid permanent renal damage (Kahan and Camardo, 2001). 

ACUTE INTRATUBULAR CRYSTAL DEPOSITION CAUSING PERMANENT RENAL DAMAGE IN THE PIG... 

The combination of guanine and allopurinol produced an acute crystal nephropathy in the pig and permanent renal damage ( ). 

Reversibility of TDF-associated renal damage is reported [204 ]. In 183 patients who were started on TDF therapy with normal renal parameters and then had renal damage after 22 (13-49.5) months from TDF discontinuation, renal parameters returned to normal values in 59% of patients, improved (without reaching normal values) in 9.8%, and did not improve in 31%. The authors suggest that since data on the reversibility of TDF-induced renal impairment are scarce, long-term prospective studies are necessary to corroborate their findings on reversibility as well as to identify those patients in whom TDF does not cause permanent renal damage. Other studies conclude that the nephrotoxicity could be irreversible [205 ]. 

Schwartz GJ, Haycock GB, Spitzer A (1976) Plasma creatinine and urea concentration in children. Normal values for age and sex. J Pediatr 88 928-830 Smellie JM (1995) The intravenous urogram in the detection and evaluation of renal damage following urinary tract infection. Pediatr Nephrol 9 213-220 Stokland E, Hellstrom M, Jacobsson B et al (1998) Evaluation of DMSA scintigraphy and urography in assessing both acute and permanent renal damage in children. Acta Radiol 39 447-452... 

Cochran, M., Moorhead, P. J. and Platts, M. (1975) Permanent renal damage with rifampicin. Lancet, 1, 1428. 

A major clinical distinction between the effects on the inner ear and the kidney is the fact that the renal effects are reversible while the effects on the inner ear are irreversible, leading to permanent loss of balance or auditory function. Furthermore, renal insults can more easily be monitored and thereby largely prevented, while monitoring of impending auditory or vestibular damage is not always possible. Ototoxic side effects frequently develop after cessation of aminoglycoside treatment, sometimes delayed by weeks. This review will therefore focus on the ototoxic side effects as a major unresolved issue in aminoglycoside toxicity. 

Acute exposure to inorganic lead can cause reversible damage to the kidneys, manifested as tubular dysfunction. Chronic exposure to lead, however, causes permanent interstitial nephropathy, which involves tubular cell atrophy, pathological changes in the vasculature, and fibrosis. The most pronounced changes occur in the proximal tubules. Indeed, lead-protein complexes are seen as inclusion bodies in tubular cells, and the mitochondria in such cells have been shown to be altered with impaired oxidative phosphorylation. Clearly, this will influence the function of the proximal tubular cells in reabsorption and secretion of solutes and metabolites. Consequently, one indication of renal dysfunction is amino aciduria, glycosuria, and impairment of sodium reabsorption. 

There is good evidence that hypercalcemia continued over a long period can cause severe and often permanent damage, especially cerebral, skeletal, and renal. In the later stages of severe cases an irreversible azotemia, possibly with hypertension and with secondary renal dwarfism, may dominate the clinical picture. Thus prognosis is materially influenced by early diagnosis and the early institution of adequate treatment. 

The long-term effects of carbon monoxide poisoning for victims who recover are less clear. Those who recover from exposure to high levels, especially if they have been unconscious, can suffer effects on the memory and the brain and heart which may last some time or even be permanent. Some victims may suffer heart attacks some time after apparent recovery or succumb to pneumonia, especially the elderly. Similarly, despite an apparent full recovery, some weeks after the poisoning the victim may suffer from effects on the brain (for example, encephalopathy) which can cause symptoms similar to Parkinson s disease or personality changes (irritability, for example) which can persist for some time. Loss of short-term memory is common. Muscle damage sometimes occurs, which can lead to renal failure. This is because the breakdown products of the muscle are excreted into the urine and overload the kidneys. These effects are most likely in those who are victims of severe poisoning. 

The characteristic features of chronic intoxication are deposition of calcium salts in various tissues. A followup study of 24 children with vitamin D intoxication (13 900-200 000 lU/day) for up to 13 years showed that 23% of the patients had permanent damage. The severity of renal, neurological, and digestive symptoms was related to the daily dose, but the final consequences depended on the duration of overdosage (7). Vitamin D intoxication has also been seen after so-called Stoss prophylaxis in children, that is the use of single very... 

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