Thyroid function surveillance in CAPD patients.

We monitored thyroid function in 75 peritoneal dialysis patients (55 +/- 15 years). A total of 20 (27%) were hypothyroid; 9 were diagnosed about the time of initiation of dialysis, and 11 prior to onset of renal failure. Thyroid function surveillance found an increase in serum thyrotropin (TSH) concentration to hypothyroid values in only one patient. On replacement therapy serum thyroxine was similar in euthyroid and hypothyroid patients (6.94 +/- 1.69 vs 6.52 +/- 1.65 micrograms/dL, respectively; p = 0.380), but TSH was higher in hypothyroid patients (5.61 +/- 5.67 vs 2.59 +/- 1.49 microU/mL, respectively; p = 0.001). Serum creatinine (8.6 +/- 3.1 vs 11.4 +/- 5.1 mg/dL, respectively; p = 0.049) and albumin concentrations (3.76 +/- 0.47 vs 3.33 +/- 0.71 g/dL, respectively; p = 0.006) were lower in hypothyroid than euthyroid patients. Hyperthyroid patients had higher serum triglyceride concentrations than euthyroid patients (306 +/- 176 vs 189 +/- 122 mg/dL, respectively; p = 0.013). Parathyroid hormone (PTH) was lower in hypothyroid than normothyroid patients (108 +/- 80 vs 261 +/- 265 pg/mL, respectively; p = 0.032). No differences were observed in serum calcium, phosphorus, and alkaline phosphatase. We conclude that hypothyroidism is common in peritoneal dialysis patients, usually antedates dialysis therapy, results in lower serum albumin and creatinine concentrations and higher serum triglyceride concentrations, is associated with lower serum PTH concentrations, and that thyroid function surveillance is not necessary in the absence of symptoms suggestive of hypothyroidism.

Effect of diet composition on renal morphology in diabetic rats.

Streptozotocin-induced diabetic rats were fed rodent diets with standard (4.5%) or high (10%) polyunsaturated fatty acid content for up to 12 months. Diabetic rats fed a standard diet developed thickening of glomerular basement membrane (GBM) when compared to similarly fed controls (285 +/- 21 vs. 243 +/- 18 nm, respectively; p = 0.0003). No differences in GBM thickening were observed between control and diabetic rats fed high-fat diets (188 +/- 23 vs. 195 +/- 21 nm, respectively; p = n.s.). Regardless of diabetes, all rats fed high polyunsaturated fat diets had decreased GBM thickness compared to standard-fed rats (p = 0.0001). Glomerular and mesangial volumes were similar in control and diabetic rats fed standard or high fat diets. Diets high in polyunsaturated fatty acids prevent GBM thickening in diabetes and reduce GBM thickness in control rats.

Glomerular pyrimidine metabolism in experimental diabetic nephropathy.

Glomerular uracil nucleotide metabolism was studied in vivo in control and diabetic rats 48 h after the injection of streptozotocin. The animals were infused for 2 h with 3H-orotate and the fraction of infused dpm incorporated into glomerular uracil nucleotides and RNA/mg of glomerular DNA was calculated. Diabetic glomeruli showed an increase in RNA/DNA compared to controls (p less than 0.05) and a greater incorporation of 3H-orotate into uracil nucleotides and RNA. These changes were reversed by insulin therapy. In separate experiments the renal cortical uracil nucleotide pool was expanded by feeding chow supplemented with 0.5% orotate to rats for 6 months. Normal animals fed orotate developed significant glomerular basement membrane thickening (p less than 0.01) when compared to age-matched controls, which was morphologically indistinguishable from that of diabetics. Orotate feeding also produced further basement membrane thickening in diabetic rats. These results suggest that early diabetes is characterized by an increase in glomerular uracil nucleotides, and that chronic expansion of the uracil nucleotide pool is associated with glomerular basement membrane thickening.