The previously reported detrimental effects of pregnancy on the course of membranoproliferative glomerulonephritis type II (MPGN type II) are limited and are usually considered to be mild. Based on these reports, a 19-year-old female with the diagnosis of MPGN type II who had stable renal function (creatinine 0.9 mg/dl) and a mild nephrotic syndrome with hypertension for 5 years of close follow-up was advised to complete her pregnancy. After a full-term pregnancy, complicated only by moderate nephrotic syndrome, a healthy female infant was born. Two weeks after delivery, the patient presented with acute renal failure and malignant hypertension, without evidence of hemolysis of hepatic failure. Immunologic parameters, including, C3, C4, antinuclear antibodies, circulating immune complexes as well as antibodies to glomerular basement membrane antigen and tubular basement membrane antigen were negative. Peritoneal dialysis was initiated and a renal biopsy was performed which showed MPGN type II with 50% crescents. Despite pulse therapy with methylprednisolone, renal function did not improve, resulting in the need for chronic dialysis. Although no specific nephritogenic mechanism was shown, the course of this patient should be considered when counseling female patients with MPGN type II, regarding the possibility of pregnancy exacerbating their disease, or resulting in rapidly progressive renal failure.
Changes in intestinal calcium absorption, calcium deposition into egg shell, and intestinal, renal and uterine calcium-binding protein (CaBP) in laying hens were related to changes in 25 hydroxycholecalciferol-1-hydroxylase activity (1-hydroxylase), or to the supplementation of 1alpha-hydroxycholecalciferol (1alpha-OH-CC). The onset of egg production resulted in an increased kidney 1-hydroxylase activity and intestinal and uterine CaBP. Renal concentrations of CaBP remained unchanged. Intestinal calcium and phosphorus absorption, during the period of egg shell formation, and duodenal calcium-binding protein (CaBP), were higher in 1alpha-OH-CC-fed than in cholecalciferol-fed hens. Renal or uterine CaBP and calcium deposition into the egg shell did not fluctuate with the vitamin D source or concentration. 1alpha-OH-CC injection into non-laying Nicarbazinfed hens resulted in an increase in intestinal but not renal or uterine CaBP concentrations. It is suggested that (a) CaBP in various organs responded independently to the same stimuli; and (b) calcium deposition into egg shell and uterine CaBP level are not related to kidney 1-hydroxylase activity or concentration of 1,25 dihydroxycholecalciferol.
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