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Biomedical subjects

C J Van Den Berg

Publications and source records attributed to C J Van Den Berg.

8 recordsLinked to original sources

Idiopathic hypercalciuria: hydrochlorothiazide decrease urinary calcium without altered renal response to parathyroid hormone.

Hydrochlorothiazide (HTZ) therapy reduces the urinary excretion of calcium (UCa V) in patients with idiopathic hypercalciuria (IH). To test the role of parathyroid hormone (PTH), namely the possibility that HTZ sensitizes the kidney to PTH as the sole or contributory cause of decreased UCa V associated with HTZ therapy, we measured urinary excretion of calcium (UCa V) and cAMP (UcAMP V), the tubular reabsorption of phosphate (TRP), plasma immunoreactive PTH, and the renal response to infused PTH (change in UcAMP V and TRP) in 10 patients with IH. Patients were studied before (control) and after 4 weeks of treatment with HTZ (100 mg/day). HTZ therapy significantly reduced UCa V (mean change, -122 +/- 19 mg/24 h). The UcAMP V, TRP, and plasma levels of calcium, phosphorus, and immunoreactive PTH were initially within the normal range and did not change significantly during HTZ therapy. PTH infusion resulted in a significant increase in the UcAMP V and a significant decrease in TRP during both control and HTZ therapy studies. There was, however, no significant difference in the degree of these renal responses to PTH infusion during the control vs. HTZ therapy studies. We conclude that the hypocalciuric effect of HTZ in patients with IH is independent of changes in PTH secretion, and that HTZ does not cause general sensitization of the nephron, namely proximal tubules, to PTH, as assessed by an increase in UcAMP V and a decrease in TRP.

Calcium

Glutamine therapy of cystinuria.

We studied the urinary excretion of cystine, acids, and cystine crystalluria in five patients with homozygous cystinuraia before and during oral glutamine therapy. Oral glutamine did not change the absolute urinary excretion or fractional excretion of cystine in our patients and did not significantly affect urinary pH. Cystine crystalluria was present before and during oral glutamine therapy.

Administration, Oral

Orthophosphate therapy decreases urinary calcium excretion and serum 1,25-dihydroxyvitamin D concentrations in idiopathic hypercalciuria.

Orthophosphate treatment of patients with idiopathic hypercalciuria reduces the urinary excretion of calcium. To examine the role of altered vitamin D metabolism in reducing the renal excretion of calcium, we studied 11 patients with idiopathic hypercalciuria before and after 2 weeks of treatment with oral neutral orthophosphate (2 g phosphorus/day). Variables measured were urine calcium and phosphorus and seseserum calcium, phosphorus, immunoreactive parathyroid hormone, and 1,25-dihydroxyvitamin D [1,25-(OH)2D]. Oral phosphate treatment significantly decreased urine calcium excretion [mean change (delta), -123 mg/24 h], increased urine phosphorus (mean delta, serum levels of 1,25-(OH)2D (mean delta, -22 pg/ml). Pretreatment levels of 1,25-(OH)2D were high when compared with levels in age-matched controls, whether assessed as the arithmetic mean (57 vs. 33 pg/ml; P < 0.025), the logarithmically normalized (42 vs. 27 pg/ml). Phosphate treatment decreased serum levels of 1,25-(OH)2D to a mean of 35 pg/ml (logarithmically normalized mean, 22 pg/ml; median, 21 pg/ml), values not significantly different from those of normal controls. Serum calcium and phosphorus concentrations were not changed by treatment. Serum immunoreactive parathyroid hormone values increased minimally within the normal range (mean delta, +2 microleq/ml; P <0.025). We conclude that the effect of oral phosphate therapy in decreasing urinary calcium excretion may involve the reduced synthesis of 1,25-(OH)2D, independent of altered parathyroid function.

Calcitriol

Diuretics: role of sodium balance.

Diuretics are commonly prescribed for a wide variety of clinical problems, including hypertension, extracellular volume excess, and disorders of calcium metabolism. Although natriuresis with altered sodium balance is not always the therapeutic goal, this feature of the diuretics is essential for optimal results, irrespective of the clinical problem.

Acute Kidney Injury

Clinical evaluation of renal lithiasis.

Determining metabolic activity in urolithiasis may avoid excessive laboratory tests and unnecessary treatment. A simple regimen such as increased oral fluids is often effective therapy in metabolically inactive disease. Most cases of renal lithiasis are idiopathic, but a complete examination and laboratory work-up will usually establish an accurate etiologic diagnosis.

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