Chronic renal failure modifies the morphology and dynamics of the growth plate (GP) of long bones. In young uremic rats, the height of cartilage columns of GP may vary markedly. The reasons for this variation are unknown, although the severity and duration of renal failure and the type of renal osteodystrophy have been shown to influence the height of GP cartilage. Expansion of GP cartilage is associated with that of the hypertrophic stratum. The interference of uremia with the process of chondrocyte differentiation is suggested by some morphological features. However, analysis by immunohistochemistry and/or in situ hybridization of markers of chondrocyte maturation in the GP of uremic rats has yielded conflicting results. Thus, there have been reported normal and reduced mRNA levels for collagen X, parathyroid hormone/parathyroid hormone-related peptide receptor, and matrix metalloproteinase 9, as well as normal mRNA and protein expression for vascular endothelial growth factor and chondromodulin I, peptides related to the control of angiogenesis. In addition, a decreased immunohistochemical signal for growth hormone receptor and low insulin-like growth factor I mRNA in the proliferative zone of uremic GP are supportive of reduced chondrocyte proliferation. Growth hormone treatment improves chondrocyte maturation and activates bone metabolism in the primary spongiosa.

To understand the changes induced by uremia in the epiphyseal growth plate, two studies were performed in young rats. In study 1, the morphological features of the tibial growth cartilage of stunted rats with different degrees of reduction of renal function were analyzed 2 weeks after nephrectomy and compared with control rats. There was a negative ( r=-0.549, P<0.05) correlation between serum urea nitrogen (SUN) concentrations and longitudinal growth rate. The heights (mean+/-SEM) of growth cartilage (564+/-32 vs. 366+/-9 microm) and its hypertrophic zone (321+/-25 vs. 157+/-6 microm) were greater ( P<0.05) in uremic than control rats and were highly and positively correlated ( r=0.604, P<0.03 and r=0.706, P<0.01) with SUN levels. In study 2, the time course of growth plate alterations was investigated in uremic rats sacrificed 1 (NX-1), 2 (NX-2), and 4 weeks (NX-4) after nephrectomy compared with their corresponding control animals (C-1, C-2, C-4). Growth cartilage and hypertrophic zone heights were greater in NX-2 (533+/-60 and 264+/-32 microm) than in C-2 (345+/-10 and 131+/-11 microm), with no significant differences in the other groups. This report shows that enlargement of the growth plate and its hypertrophic stratum is greatly, although not exclusively, influenced by the severity and duration of renal insufficiency.

In experimental uremia, expansion of growth cartilage does not result from increased or persistent expression of ChM-I or from reduced VEGF expression at the cartilage-metaphyseal bone interphase. GH treatment does not modify ChM-I and VEGF expressions.

The outcome of ischemic acute renal failure (IARF) is better in young than adult rats. Insulin-like growth factor I (IGF-I) treatment may increase mortality of adult rats with IARF, probably because of an exaggerated inflammatory response. We report the response to IGF-I therapy in young rats with IARF. Male rats, aged 28+/-1 days, with IARF were given subcutaneous IGF-I, 50 microg/100 g at 0, 8, and 16 h after reperfusion (IGF) or were untreated (ARF). Sham-operated rats were used as controls. At 2 and 7 days after ischemia, serum urea nitrogen and histological damage score, cell proliferation, apoptosis, neutrophil infiltration, and IGF-I receptor mRNA in kidneys were analyzed. The degree of renal failure, mortality rate, histological damage, cell proliferation, and neutrophil infiltration were not different between IGF-I and ARF rats. Hence, short-term IGF-I treatment did not modify the course of IARF in young rats.

Keywords Severe acute abdominal pain · Steroid-sensitive idiopathic nephrotic syndrome Sirs, A 14-year-old white male was admitted to our hospital because of severe abdominal pain of acute onset. No diarrhea or vomiting had been noted. Eleven years before he had been diagnosed with steroid-sensitive idiopathic nephrotic syndrome. He had presented with 14 relapses, the last 19 months prior to admission. No medication other than prednisone had ever been used to induce remission of proteinuria. In an attempt to avoid relapses, the boy had been placed on prophylactic treatment with 5 mg of oral prednisone every other morning for the last 6 months. Because of the steroid sensitivity, a renal biopsy had not been performed. The family history was negative for renal diseases and polycythemia.Physical examination revealed minimal palpebral edema, diffuse abdominal pain without signs of peritoneal inflammation, normal chest auscultation, and good peripheral circulation. His weight was 68.5 kg. Blood pressure was 100/55 mmHg. Laboratory tests showed blood hemoglobin 20.5 g/dl, hematocrit 62.2%, white blood cell count 33,100/µl, platelet count 443,000/µl, serum albumin 13.5 g/l, serum total proteins 35.5 g/l, serum sodium 128 mEq/l, serum urea 82 mg/dl, serum creatinine 1.4 mg/dl, cholesterol 359 mg/dl, serum triglycerides 296 mg/dl, and serum osmolality 285 mosmol/kg. Activated partial thromboplastin time (32.3 s), prothrombin time (11.7 s), and levels of plasma fibrinogen (534 mg/dl) were within normal ranges. Urinalysis revealed proteinuria, microhematuria, and granular casts. Urinary volume (24-h) was 620 ml (15.5 ml/m 2 per hour), creatinine clearance 119 ml/min per 1.73 m 2 , natriuresis 2 mEq/l, protein/creatinine ratio 7.9 mg/mg, and urine osmolality 899 mosmol/kg. His peripheral plasma renin activity was 95.4 ng/ml per hour (supine) (reference values 1.3-4 ng/ml per hour) and serum erythropoietin concentration was 8.6 mU/ml (reference values 5-25.2 mU/ml). Doppler ultrasonography of inferior cava and renal veins was normal. On admission, treatment was started with 80 mg/day of i.v. methylprednisolone followed by 80 mg/day of oral prednisone, 200 mg/day of oral aspirin, 40 mg/day of subcutaneous low molecular weight heparin, and ranitidine 50 mg t.i.d. i.v. for 3 days and thereafter 150 mg b.i.d. by the oral route. On the 3rd day of admission, the patient was free of symptoms, his weight was 67.5 kg, proteinuria had decreased, and blood hemoglobin was 17.5 g/dl. He was discharged on the 5th day of admission. During follow-up, proteinuria became negative and hemoglobin returned to normal values of 12.8 g/dl.The highly elevated concentrations of hemoglobin and hematocrit found in the patient presented here are rarely observed in patients with nephrotic syndrome, even during the first episode of nephrotic syndrome when the time elapsing from the appearance of proteinuria until a correct diagnosis is made is usually much longer than that required to identify the relapses. Hypovolemia and hemoconcentration, consistent wit...