No abstract

The effect of treatment of male osteopomsis is not well documented. We studied prospectively, in an uncontrolled single blind study, the effect of a ?--year treatment with cyclic etidronate (400 mg/d during 2 weeks every 3 months) and calcium (500 moJd during 10 weeks every 3 months) in 64 men with idiopathic (n=29) or secondary (n=35) osteopenia. Vertebral fractures were present in 41 patients. The remaining 23 patients had osteopenia (T-score of the spine <~ Bone density (BMD) was measured by dual-energy x-ray absorptiometry in the spine and the femoral neck. in serum, bone-specific alkaline phosphatase (BSAP) and osteocalcin (Oc) were measured by competitive immunoassay (Alkphase-BTM; Novocalcin TM, Metra Biosystems Inc.) in a random subgroup of 20 patients. BMD increased by 6% in the lumbar spine (p<0.001), and in the femural neck by 3% (NS). After 2 years of treament, 79% positive responders were found in the lumbar spine (p<0.001) and 68% in the hip (p

The patterns of phosphate excretion in man with advancing chronic renal disease are well established. Although phosphate clearance decreases with time, it falls proportionately less than glomerular filtration rate, and the ratio of phosphate clearance to GFR increases as the disease advances (1). Thus the average rate of phosphate excretion per residual nephron increases as the nephron population diminishes, and the onset of hyperphosphatemia thereby is delayed. The explanation for this sequence is of considerable theoretical interest. The major possibilities are two: 1) The change could reflect the operation of a control system geared either to maintain external phosphate balance or to maintain plasma phosphate concentrations constant; 2) the relative phosphaturia per nephron could be a consequence of uremia or of the abnormalities in residual nephrons or both. These studies represent an attempt to distinguish between these two interpretations using the dog with intrinsic renal disease as the experimental model. The experiments also were designed to delineate the general characteristics of a control system, should one exist. phate intake of at least 0.5 g. A preliminary bladdersplitting operation was performed to permit the quantitative collection of urine from the individual kidneys without recourse to ureteral catheterization (2). Thereafter, unilateral pyelonephritis was induced by a technique described previously (3). In five dogs, the diseased kidney was studied in the presence of the control kidney, and the functions of the two organs were compared. These experiments were similar in design to those described in a previous publication (4) and were performed to verify the previous results in the present animals. In 27 dogs, the control kidneys were removed to permit investigation of the diseased kidneys under environmental conditions varying from moderate azotemia to severe uremia. Methods

In 30% of cases nephrotic syndrome is caused by membranous glomerulonephritis (MG). Protein accumulation in glomeruli leads to progressive loss of kidney function and damage of structure in MG. The role of tissue proteolytic systems and growth factors in this process is not known. The purpose of the study was to estimate urine cathepsin B, collagenase activity and urine excretion of TGF-beta 1 and fibronectin in MG. Cathepsin B activity was greater in the urine of MG patients than in the control group (10.58 +/- 8.73 pmol AMC/mg creatinine per min-1 vs control 7.11 +/- 2.05 pmol AMC/mg creatinine per min-1; P < 0.05). Urine collagenase activity was higher in the group of patients than in the control group (8.59 +/- 4.26 pmol AMC/mg creatinine per min-1 vs control 3.84 +/- 2.09 pmol AMC/mg creatinine per min-1 P < 0.02). Urine excretion of fibronectin (45.60 ng/mg creatinine vs control 10.30 ng/mg creatinine; P < 0.04) and TGF-beta 1 levels in the urine were higher than in controls (283.55 +/- 248.13 pg/ml vs 36.11 +/- 48.01 pg/ml; P < 0.01). Results suggest glomerular overproduction of TGF-beta 1 and urinary leak of proteolytic enzymes (PE). This may result in decreased glomerular PE activity in MG and, with time, may lead to protein accumulation in renal glomeruli and to progressive loss of kidney function and damage of structures as the course of MG progresses. PE urine composition as well as ECM protein and cytokine urine excretion may allow noninvasive glomerulopathy course monitoring in humans in the future.