Biomedical subjects

C Skurla

Publications and source records attributed to C Skurla.

4 recordsLinked to original sources

PubMed1985

Prevention of recurrent calcium stone formation with potassium citrate therapy in patients with distal renal tubular acidosis.

Distal renal tubular acidosis is a common cause of intractable calcium nephrolithiasis. We examined the effect of oral potassium citrate therapy in 9 patients with incomplete distal renal tubular acidosis diagnosed on the basis of an abnormal response to an oral ammonium chloride load. Patients were studied during a control phase and after 3 months of potassium citrate treatment (60 to 80 mEq. daily). Potassium citrate caused a significant increase in urinary pH and urinary citrate, and a decrease in urinary calcium. The urinary relative saturation ratio of calcium oxalate significantly decreased during treatment, while that of brushite did not change. Potassium citrate also was shown to inhibit new stone formation. During a mean treatment period of 34 months none of the 9 patients had new stones, although 39.3 plus or minus 79.7 (standard deviation) stones per patient formed during the 3 years preceding treatment. The results support the potential clinical advantage of potassium citrate therapy in patients with distal renal tubular acidosis and recurrent calcium nephrolithiasis.

Acidosis, Renal Tubular↗

PubMed1985

Graphic display of urinary risk factors for renal stone formation.

From the analysis of various urinary constituents and the estimation of urinary saturation of stone-forming salts, it is now possible to identify risk factors responsible for or contributing to stone formation. Metabolic factors included calcium, oxalate, uric acid, citrate and pH. Environmental factors were total volume, sodium, sulfate, phosphate and magnesium. Physicochemical factors represented saturation of calcium oxalate, brushite, monosodium urate, struvite and uric acid. A scheme for graphic display of risk factors was developed to allow ready visual recognition of important risk factors presumed to cause stone formation. This graphic display had diagnostic use as well as practical value in following response to treatment. For example, a low urinary pH and high urinary concentration of undissociated uric acid could be discerned readily in cases of uric acid lithiasis, as were high urinary pH and exaggerated urinary supersaturation of struvite in cases of infection lithiasis. In a patient with absorptive hypercalciuria and hypocitraturia treatment with thiazide and potassium citrate could be shown to abolish high risks (hypercalciuria, hypocitraturia and relative supersaturation of calcium oxalate) displayed before treatment.

Calcium↗

PubMed1984

Augmentation of renal citrate excretion by oral potassium citrate administration: time course, dose frequency schedule, and dose-response relationship.

The time course, dose frequency schedule, and dose-response relationship of the citraturic response to orally administered potassium citrate was examined in 22 normal volunteers and 21 patients with uric acid or calcium nephrolithiasis. The slow-release (wax matrix) preparation of potassium citrate produced a rapid and sustained rise in urinary citrate lasting for up to 12 hours following a single oral administration. Probably owing to this prolonged action, the slow-release preparation when given in a twice-daily or thrice-daily schedule at a dosage of 60 meq or 3.78 Gm citrate/day virtually eliminated the normally wide circadian fluctuation in urinary citrate and maintained urinary citrate at a higher, more constant level throughout the day. The liquid preparation of potassium citrate was less effective in this regard. However, the two preparations of potassium citrate caused an equivalent rise in total 24-hour urinary citrate. When 24-hour excretions of citrate were examined, urinary citrate was shown to reach its peak level by the second day of potassium citrate treatment and to return to the pretreatment level by the second day after the treatment was stopped. The rise in urinary citrate produced by treatment was directly proportional to the dose of potassium citrate. In most hypocitraturic patients with renal stones, potassium citrate 60 meq/day restored normal urinary citrate (greater than 320 mg/day).

Administration, Oral↗

PubMed1983

Low urinary citrate excretion in nephrolithiasis.

The urinary citrate excretion was examined in patients with nephrolithiasis who were categorized on the basis of different physiologic or metabolic abnormalities. A wide prevalence of low citrate excretion (hypocitraturia) was observed, with over one half of our patients with stones exhibiting it. Hypocitraturia was found in all patient categories except primary hyperparathyroidism and hyperuricosuric calcium oxalate nephrolithiasis. As expected, hypocitraturia was present in renal tubular acidosis and in enteric hyperoxaluria. However, urinary citrate was also low in absorptive and renal hypercalciurias, and in patients in whom an acid-base disturbance was clearly excluded.

Acidosis, Renal Tubular↗