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Renal handling of citrate in children with various kidney disorders
Insights
Urinary citrate excretion varies in pediatric kidney diseases. Reduced citrate is seen in acute glomerulonephritis and renal failure, while increased levels occur in cystinosis and Fanconi syndrome.
Area of Science:
- Nephrology
- Pediatric Nephrology
- Urology
Background:
- Urinary citrate plays a role in preventing kidney stones.
- Citrate metabolism is complex and can be affected by various kidney disorders.
Purpose of the Study:
- To investigate citrate (CIT) excretion in children with diverse kidney conditions.
- To understand the relationship between citrate handling and glomerular filtration rate (GFR).
Main Methods:
- Measured 24-hour urinary citrate excretion in children with kidney disorders and controls.
- Assessed renal handling of citrate under inulin clearance conditions.
- Performed acid loading tests to evaluate urinary citrate response.
Main Results:
- Normal citrate excretion was observed in urinary tract infection, idiopathic urolithiasis, and idiopathic hypercalciuria without renal dysfunction.
- Reduced citrate excretion was found in acute glomerulonephritis, distal renal tubular acidosis, and chronic renal failure.
- Increased citraturia was noted in cystinosis and idiopathic de Toni-Debré-Fanconi syndrome.
- Citrate clearance correlated with GFR; tubular reabsorption decreased significantly at lower GFR levels.
- Acid loading lowered citraturia in controls and tubular disorders, with the lowest excretion in incomplete renal tubular acidosis with magnesium wasting.
Conclusions:
- Urinary citrate excretion patterns differ across pediatric kidney diseases.
- Reduced tubular reabsorption of citrate may indicate early renal insufficiency.
- Citrate metabolism is significantly impacted by renal tubular dysfunction and acid-base balance.
Abstract:
Citrate (CIT) excretion was measured in 24 h urine of children with various kidney disorders and controls. It was normal in urinary tract infection, idiopathic urolithiasis, and idiopathic hypercalciuria in the absence of renal dysfunction, but reduced in acute glomerulonephritis, distal renal tubular acidosis, and chronic renal failure. Increased citraturia was observed in cystinosis and in idiopathic de Toni-Debré-Fanconi syndrome. Renal handling of CIT was studied in 45 children with various chronic kidney disorders under standard inulin clearance conditions. CIT clearance correlated well with GFR above 50 ml/min/1.73 m2. At lower levels, percent tubular reabsorption of CIT decreased rapidly, reaching levels between 17% and 41% at GFR less than 10 ml/min/1.73 m2; this disproportionate fall might be related to reduced renal CIT utilization at a relatively early stage of renal insufficiency. During acid loading tests, citraturia was lowered, with a decrease of both urinary pH and plasma bicarbonate in tubular disorders and in controls. The lowest CIT excretion was measured in incomplete renal tubular acidosis with magnesium wasting. The findings are discussed in view of recent physiological data on renal metabolism of CIT.