Glomerular function

Chia KS, Jeyaratnam J, Tan C, et al. 1995a. Glomerular function of lead-exposed workers. Toxicol Letters 77 319-328. 

Thus, animal data indicate that nickel can damage glomerular function and cause renal tubular damage, while data in humans indicate that occupational exposure to nickel can result in tubular damage without affecting glomerular function. It is unlikely that environmental exposure or exposure at hazardous waste sites will result in renal effects. 

There is no final consensus on whether normal use of lithium, without any episode of toxicity (the vast majority of patients), may result in permanent renal impairment. Polyuria occurs in 20-40% and is due to inhibition of antidiuretic hormone (ADH) by lithium. It usually resolves on cessation of lithium as do any effects on glomerular function. Interference with thyroid function is due to inhibition of the action of thyroid stimulating hormone (TSH) and is easily managed by administration of thyroxine. Lithium is contraindicated during pregnancy (major vessel anomalies in fetus) and breastfeeding. 

The major eicosanoid products of the renal cortex are PGE2 and PGI2. Both compounds increase renin release normally, however, renin release is more directly under Bi adrenoceptor control. The glomeruli synthesize small amounts of TXA2 but this potent vasoconstrictor does not appear to be responsible for regulating glomerular function in healthy humans. 

P3. Pavenstadt, H., Roles of the podocyte in glomerular function. Am. J. Physiol. 278, F173-F179... 

Renal function is limited at birth because the kidneys are anatomically and functionally immature. In full-term newborns, glomerular filtration rate (GFR) is 10-15 mL/min/m, and in premature infants the GFR is only 5-10 mL/min/m. GFR doubles by 1 week of age, because of a postnatal drop in renal vascular resistance and increase in renal blood flow, and reaches adult values by 1 year of age (Figure 23.6) (40,41). A glomerular/tubular imbalance is present in newborns, because glomerular function matures more... 

Kidneys Dysfunction of the proximal tubule may occur as a late manifestation of Wilson s disease. Epithelial flattening, a loss of the brush-border membrane, mitochondrial anomalies and fatty cellular changes can be observed. These findings are, in turn, responsible for proteinuria with a predominance of hyperaminoaciduria (L. UzMAN et al., 1948). Enhanced calciuria and phosphat-uria may cause osteomalacia as well as hypoparathyroidism. (329, 344) Glucosuria and uricosuria, if present, are without clinical relevance. Due to decreased bicarbonate resorption, tubular acidosis may occur, with a tendency towards osteomalacia as well as the development of nephrocalcinosis and renal stones (in some 15% of cases). (344, 356, 392) The intensity of the copper deposits in the kidneys correlates closely with the cellular changes and functional disorders. The glomerular function is not compromised, with the result that substances normally excreted in the urine are not retained. 

The ideal criteria for interpretation of enzymuria [168] include the following (i) to evaluate glomerular function the enzyme should he present in blood, absent in renal tissue and have a molecular size that precludes its filtration (ii) to evaluate tubular reabsorption the enzyme should be present in blood, absent from renal tissue, have a molecular weight that allows it to be freely filtered and be reabsorbed by the tubule and (iii) to evaluate anatomical and functional condition of the tubular epithelium the enzyme should be restricted to the renal tissue. 

Nitric oxide, endothelium-derived hyperpolarizing factor and prostaglandins Renal and cardiac fibrosis Glomerular function in the IPRK Disadvantages of the IPRK model Advantages of the IPRK model... 

Schor N, Ichikawa I, Rennke EIG, Troy JE, and Brenner BM. Pathophysiology of altered glomerular function in aminoglycoside-treated rats. Kidney Int 19 288-296,1981. 

Recently AmB and ABCD were administered in rats, and both drugs showed no decrease in glomerular function they however caused damage to renal tubuh. Toxicity was more pronounced with AmB than ABCD [169,170]. 

Schor N, ichikawa I, Rennke HG,Troy JL, Brenner BM. Pathophysiology of altered glomerular function In amlnoglycoside-treated rats. Kid ney I nt 1981 19 288-92. 

Depaulo JR Jr, Correa EJ, Sapir DG. Renal glomerular function and long-term lithium therapy. Am J Psychiatry 1981 138 324-327. 

Comment changes reflect cellular toxicity and/or altered glomerular function Glucosuria/amino aciduria... 

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