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Renal tubular defects in recurring bilateral nephrolithiasis
Clinical Nephrology
|August 1, 1976
Summary
Patients with kidney stones and chronic pyelonephritis often have incomplete distal renal tubular acidosis, affecting their ability to conserve sodium and water.
Area of Science:
- Nephrology
- Metabolic Studies
- Renal Physiology
Background:
- Bilateral recurrent calcium-containing renal staghorn calculi and chronic pyelonephritis can lead to obstructive nephropathy.
- Obstructive nephropathy may impact renal function, including glomerular filtration rate (GFR).
Purpose of the Study:
- To investigate metabolic disturbances in patients with obstructive nephropathy.
- To determine the prevalence of acid-base balance defects in this patient population.
Main Methods:
- Metabolic study involving 28 patients with obstructive nephropathy (14 normal GFR, 14 mild renal insufficiency) and 10 healthy controls.
- Administration of an acute acid load (ammonium chloride) and intravenous neutral sodium phosphate infusion.
- Measurement of urine pH, titratable acid, ammonium excretion, and phosphate excretion.
Main Results:
- Patients commonly exhibited polyuria and negative sodium balance.
- An acidifying defect (high urine pH, reduced titratable acid and ammonium excretion) was observed in 64% of patients with normal GFR and 71.4% with renal insufficiency after acid load.
- Urine pH remained stable during phosphate infusion, with increased titratable acid excretion proportional to phosphate excretion.
Conclusions:
- Incomplete Type 1 (distal) renal tubular acidosis is a frequent complication of obstructive nephropathy secondary to bilateral nephrolithiasis.
- Renal tubular and collecting duct abnormalities, along with interstitial nephritis, likely contribute to the acidifying defect and impaired sodium/water conservation.