IgA nephropathy in patients with familial Mediterranean fever

Two patients with a long-standing history of familial Mediterranean fever were found to have both microscopic hematuria and proteinuria during the acute attacks. Kidney biopsies from both patients revealed diffuse mesangial proliferative glomerulonephritis with intense mesangial IgA and C3 deposits and no evidence of amyloidosis. To our knowledge these are the first 2 cases documenting the presence of mesangial IgA nephropathy in patients with familial Mediterranean fever.     

Effect of epidermal growth factor and artificial feeding in suckling rats

To evaluate the effects of epidermal growth factor (EGF) in dietary milk, a new method of delivering an artificial (EGF-deficient) formula was developed using 42 rat pups, 1-14 days of age. In a second study the effect of EGF was evaluated in suckling rats from 3-11 days of age: group 1, mother-fed; group 2, mother-fed plus daily injections of EGF (0.1 micrograms/g body weight); group 3, artificial milk fed with added EGF (62 ng/ml); and group 4, artificial milk fed without EGF. Each group consists of nine rats. In group 2 there was premature eye opening and tooth eruption and a significant reduction in body weight and weight of liver, kidney, thyroid, and thymus but an increase in length of the intestine and weights of stomach, pancreas, lung, and adrenal (p less than 0.04), when compared to group 1. Both groups 3 and 4 showed premature tooth eruption and eye opening, and their body weights and most organ weights were similar to group 2; exceptions were a smaller stomach, thyroid, thymus, lung, and adrenal, which were similar to those in group 1. In addition, intestinal length in groups 3 and 4 were similar to the mother-fed EGF-treated pups (group 2). There was no difference in intestinal length between the artificially fed pups, whether or not they received oral EGF. These findings demonstrate a new and effective technique of artificial feeding and suggest that the increase in intestinal length caused by injections of EGF (0.1 micrograms/g body weight) can also be induced by feeding an artificial milk with or without physiologic levels of EGF.     

Glutamine transport by human intestinal basolateral membrane vesicle

This study characterizes for the first time, by use of a well-validated technique, glutamine transport across human basolateral membrane vesicles. Glutamine transport represented uptake into an osmotically active intravesicular space without significant metabolism. Glutamine uptake was temperature- and pH-dependent with maximal uptake at pH 7.5, and it was mediated by sodium-dependent and -independent processes. The initial rate of uptake was linear up to 20 s, as depicted by the formula gamma (nmol/mg protein) = 0.0009 X (s) - 0.0011 (r = 0.99). Kinetic analysis of glutamine uptake at concentrations between 0.01 and 0.3 mmol/L at 5 s under sodium and potassium gradients showed a maximal transport capacity (Vmax) of 0.39 +/- 0.04 and 0.21 +/- 0.02 nmol.mg protein-1.5 s-1 for sodium-dependent and -independent processes, respectively (p less than 0.01). Km values were 0.17 +/- 0.04 and 0.06 +/- 0.2 mmol/L, respectively (p less than 0.05). Glutamine uptake under the sodium-gradient condition was electrogenic whereas under the potassium-gradient it was electroneutral. Neutral amino acids inhibited both sodium-dependent and -independent processes. This study confirms and characterizes the presence of carrier-mediated glutamine uptake at the basolateral membranes of human enterocytes.     

Light chain tubulopathy without Fanconi syndrome.

A 59-year-old white male was found to have mild proteinuriaand renal insufficiency during a life insurance test in 2003.His serum creatinine has been stable at 1.6 mg/dl since then.His 24 h urine protein was 720 mg in 2003 and 861     

Synthesis and ring transformation of pyrrolo[2,3-d][1,3]oxazine to pyrrolo[2,3-d]pyrimidines

A convenient route is reported for the synthesis of fused pyrrolo [2, 3-d] [1, 3]-oxazine and pyrrolo [2, 3-d]-pyrimidine derivatives from 2-amino-1-benzyl-3-t-butoxycarbonyl-4, 5-dimethylpyrrole.