Nephrocalcinosis

Glycinuria results from a defect in renal tubular reabsorption. The defect in primary hyperoxaluria is the failure to catabolize glyoxylate formed by deamination of glycine. Subsequent oxidation of glyoxylate to oxalate results in urohthiasis, nephrocalcinosis, and early mortality from renal failure or hypertension. 

A 55-year-old postmenopausal female develops weakness, polyuria, and polydipsia. Nephrocalcinosis is detected by a computed tomography (CT) scan. Her serum creatinine is elevated. Which of the following agents may have caused these adverse effects ... 

The answer is c. (Hardman, p 15.33.) Enthusiastic over medication with vitamin D may lead to a toxic syndrome called hy/jervitamijmsis D. The initial symptoms can include weakness, nausea, weight loss, anemia, and mild acidosis. As the excessive doses are continued, signs of nephrotoxicity are manifested, such as polyuria, polydipsia, azotemia, and eventually nephrocalcinosis. In adults, osteoporosis can occur. Also, there is CNS impairment, which can result in mental retardation and convulsions. 

Gunson, D.E., D.F. Kowalczyk, C.R. Shoop, and C.F. Ramberg, Jr. 1982. Environmental zinc and cadmium pollution associated with generalized osteochondrosis, osteoporosis, and nephrocalcinosis in horses. Jour. Amer. Veterin. Med. Assoc. 180 295-299. 

Tubulointerstitial disease Acute allergic interstitial nephritis Pamidronate Nephrocalcinosis... 

Male New Zealand rabbits displayed nephrosis of the convoluted tubules and nephrocalcinosis when given doses of 320 and 1,000 mg/kg/day hexachloroethane in methyl cellulose solution for 12 days (Weeks et al. 1979). Kidney weights were increased significantly for the 1,000 mg/kg/day dose. There were no observed effects on the kidney with a dose of 100 mg/kg/day. 

The kidney Ca level generally increased with age in all groups and fluoride feeding did not seem to have any consistent effect on the accumulation of Ca. In young rats, however, we observed an apparent increase in kidney Ca when 200 mg/kg fluoride was fed for only 6 weeks (Table V). When the fluoride level in the diet was 50 mg/kg, however, nephrocalcinosis in young rats was found to decrease (20). 

There are only a few reports on the efficacy of feverfew in an in vivo situation. Inhibition of collagen-induced bronchoconstriction in an in vivo guinea-pig model was demonstrated [56] and it was concluded that this was consistent with in vivo phospholipase A2 inhibition. In a rat model of experimentally induced nephrocalcinosis, parthenolide was shown to protect the rats against this condition. Inhibition of prostaglandin biosynthesis may have been the mechanism of action of parthenolide in this case, as prostaglandins are thought to be involved in nephrocalcinosis [57]. 

Excess vitamin D can result in hypervitaminosis D with serious vitamin D toxicity characterized by hypercalcemia and nephrocalcinosis. 

Adverse effects include headache, weakness, nausea, vomiting, dry mouth, muscle pain, constipation, somnolence, ectopic calcification, hypertension, nephrocalcinosis and weight loss. 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

Mis-localisation of annexin 2 has recently been implicated in the pathogenesis of Dent s disease. This term is now used collectively to describe what was previously four conditions that affect kidney function X-linked recessive nephrolithiasis with renal failure, X-linked recessive hypophosphatemic rickets, idiopathic low molecular weight proteinuria with hypercalciuria and nephrocalcinosis and Dent s disease. Patients with this condition present with low molecular weight proteinuria and hypercalciuria. Renal stones, nephrocalcinosis and renal failure are common late-stage developments. The condition has been attributed to abnormal acidification within endosomes of the proximal tubular cells. It is very rare and is usually caused by mutations in the voltage-dependent Cl /H+ chloride antiporter CLCN5, but occasionally in the PI4,5P2 5-phosphatase, OCRL1 (oculocerebrorenal syndrome of Lowe protein 1). 

It should be taken into account that the abundance of PolyPs in food may have some unstudied effect on health. For example, if rats were fed with a high-phosphorus diet, they developed nephrocalcinosis. This was more severe in rats fed on PolyP3 than in those fed on pyrophosphate (Matsuzaki et al., 2001). Thus, the influence of PolyPs in food on human health needs further investigations, especially in view of those diseases associated with phosphate metabolism. 

H. Matsuzaki, R. Masuyama, M. Uehara, K. Nakamura and K. Suzuki (2001). Greater effect of dietary potassium tripolyhosphate than potassium dihydrogenphosphate on the nephrocalcinosis... 

G7. Gershoff, S. N., and Andrus, S. B., Dietary magnesium, calcium, and vitamin Bg and experimental nephropathies in rats calcium oxalate calculi, apatite nephrocalcinosis. J. Nutr. 73, 308-316 (1961). 

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. 

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