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The control of the formation of crystals in biological fluids is one of the most exciting field of research involving both organic and biochemical areas. Many organisms have evolved mechanisms which minimize or avoid the effects of nucleation and crystal growth formation. One of the most important mechanism is the interaction of specific proteins, called inhibitors, with crystals which alters their habits and leads to their elimination. This article, focused on saliva, pancreatic juice and bile, reviews our present knowledge on the structure-function relationships existing between these proteins and their ability to inhibit the growth of different calcium salt crystals.

Human urine is supersaturated with respect to calcium salts especially calcium oxalate which is the major mineral phase of urinary stones. Inhibitors of crystallization prevent renal calcification in urine. Small molecular weight components account for 20% of total inhibitory activity of urine. Macromolecular inhibitors (molecular weight greater than 10 kDa) are more powerful. Recently, several macromolecules have been identified in urine, in urinary stones and in the kidney: Nephrocalcin, Tamm-Horsfall protein, Uropontin, Crystal Matrix Protein, renal Lithostathine. The role of these proteins is stressed.

We report two cases of tuberculosis in patients undergoing maintenance dialysis. In both cases Mycobacterium tuberculosis was not isolated in spite of multiple localizations and diagnosis was made with delay. Severe hypocalcemia was the main symptom in one patient, who had pulmonary, genito-urinary and spinal tuberculosis. The other patient had tuberculous lymphadenitis. The two patients survived their disease on antituberculous therapy. From the literature the authors give the actuarial data of tuberculosis occurring in patients undergoing hemodialysis.

Lithostathine is a protein of pancreatic secretion inhibiting calcium carbonate crystal growth. Antibodies to lithostathine were used to identify a related protein in urine and kidney stones. Western blot analysis of proteins extracted from concentrated normal urine or kidney stones demonstrated the presence of a protein with an apparent molecular weight of 23 kDa. The same antibodies were used in immunolocalization experiments on fresh human nephrectomy specimens cryosections. A positive signal was observed in the cells of proximal tubules and thick ascending limbs of Henle's loop. Protein extracts of renal stones inhibited calcium carbonate crystal growth. Because of its structural and functional similarities with pancreatic lithostathine, it was called renal lithostathine.

Pancreatic juice is supersaturated in calcium carbonate. CaCO3 crystal growth is controlled by lithostathine, a secretory protein synthesized by pancreatic acinar cells, first described as a constituent of pancreatic stones. It was recently reported that, in the thin descending limb of the Henle's loop, urine was supersaturated in CaCO3 (Coe FL, Parks JH: Defenses of an unstable compromise: crystallization inhibitors and the kidney's role in mineral regulation. Kidney Int. 1990: 38, 625-631. This observation suggested the presence in kidney of a similar inhibitor. In this study, we show that a protein immunologically related to lithostathine is actually present in urine of healthy subjects and in renal stones. Immunocytochemistry of kidney sections localized the protein to cells of the proximal tubules and thick ascending limbs of the Henle's loops. Protein extracts of renal stones inhibited CaCO3 crystal growth in vitro and this inhibition was significantly lifted by incubating the extracts with antibodies to lithostathine. The protein is not immunologically related to nephrocalcin. Because of its structural and functional similarities with pancreatic lithostathine, it was called renal lithostathine.

Analysis of urinary protein composition is an important tool in studies on renal physiology and physiopathology. Urine is, however, a complex mixture containing, besides protein, a variety of compounds such as salts, peptides, oligosaccharides, and glycosaminoglycans. Some of these compounds interfere with the electrophoretic migration of protein in sodium dodecyl sulfate-polyacrylamide gels and prevent correct analysis of the protein pattern. We describe a simple method for extracting urinary proteins that considerably improves their electrophoretic migration and subsequent immunodetection. This treatment involves ammonium sulfate fractionations (for precipitating proteins), EDTA (for inhibiting protein aggregation), and HCl hydrolysis (for removing glycosylaminoglycans). Recovery during extraction was found to be almost quantitative for total protein and three representative proteins: albumin, alpha 1-glycoprotein acid, and beta 2-microglobulin.

Muscular disorders are usual in hypothyroidism, but hypothyroid myopathy is most often limited to myalgias, muscle stiffness and cramps with sometimes elevated levels of muscle enzymes. We report a case of acute renal failure related to rhabdomyolysis, which complicated hypothyroïd myopathy. Thyroid hormone replacement therapy improved thyroid and renal function, and reversal rhabdomyolysis. Hypothyroidism appears to be an authentic cause of rhabdomyolysis and should be eliminated in all patients with serum muscle enzyme increase.

The association of membranous glomerulonephritis with carcinoma and minimal change disease with Hogkin's disease are well established. In contrast cancer and crescentic glomerulonephritis is an uncommon association. We report a patient with gastric carcinoma who developed synchronously acute renal failure due to crescentic glomerulonephritis. Corticosteroid therapy, plasma exchanges and tumor resection was associated with a regression of renal failure. Carcinoma must be considered as a possible cause of crescentic glomerulonephritis.

Cyclosporine A at pharmacological doses decreases the rate and yield of ATP synthesis in rat mitochondria. This action seems to be due to the mitochondrial calcium storage induced by the drug. If such an effect occurs in vivo, the ATP deficit will affect calcium extrusion pumps, so triggering vasoconstriction which is the major side effect of Cyclosporine A. Calcium antagonists (Nifedipine and Verapamil) at least partially correct this effect on ATP synthesis: this finding may be related with the beneficial clinical effect conferred on Cyclosporine A toxicity by calcium antagonists. This effect of calcium antagonists may be due to an interaction with Cyclosporine A at the level of mitochondrial calcium efflux.

Hyperkaliema at 6 mmol/l was discovered in a 30-year old man during routine examination. Further investigations showed that the hyperkaliaemia was associated with hyperchloraemic acidosis, stimulable hyporeninaemia and relative hypoaldosteronism in relation to the hyperkaliaemia. Renal and adrenal functions were normal. The finding of 3 identical cases in a French family of 9 persons led to the diagnosis of Gordon's syndrome, a rare hereditary metabolic disorder with a controverted physiopathology.

The impact of nephropathy on the diabetic pregnancy is reviewed. Proteinuria and blood pressure increase, this increase is generally reversible after delivery and the progression of renal insufficiency remains generally unchanged. Arterial hypertension seems to be the only contraindication to pregnancy in a diabetic women with nephropathy. Percentage of premature delivery by cesarean section is high and increases the frequency of hypotrophy and post natal complication especially the respiratory distress of the new born. However, the progress in pediatric intensive care allow the same prognostic what so ever the diabetic women had renal insufficiency or not. The follow up of these pregnancies is assumed by a team of diabetologist, nephrologist and gynecologist. Short acting insulin is mandatory, hypotensive drugs must be used carefully. In spite of the low number of published cases a pregnancy may be successful in a diabetic women after renal transplantation or even after renal and pancreatic transplantation.