[SOLITARY KIDNEY - IS IT TOO LITTLE?]

Area of Science:

• Nephrology
• Pediatric Nephrology
• Genetics

Background:

• Solitary functioning kidney (SFK) affects 1 in 2000 live births, often associated with unilateral renal agenesis (URA) or nephrectomy.
• URA can present with various anomalies and may have a genetic component, with 10% of cases having affected family members.
• SFK triggers compensatory hyperfiltration, which can lead to long-term nephron loss and kidney function decline.

Purpose of the Study:

• To highlight the long-term risks associated with solitary functioning kidney (SFK).
• To identify factors influencing the risk of progressive renal damage in SFK.
• To emphasize the importance of lifelong monitoring and early intervention for individuals with SFK.

Main Methods:

• Review of existing literature on solitary functioning kidney (SFK) and unilateral renal agenesis (URA).
• Analysis of factors contributing to compensatory hyperfiltration and nephron loss.
• Identification of clinical indicators for reduced nephron number and progressive renal damage.

Main Results:

• The number of nephrons in the SFK, though not directly measurable, is a primary determinant of future risk.
• Factors like prematurity, SGA birth weight, urological anomalies, and lack of compensatory hypertrophy suggest reduced nephron count.
• Acquired factors such as nephrotoxin exposure, obesity, and high salt/protein intake exacerbate kidney damage risk.

Conclusions:

• Lifelong follow-up from early childhood is essential for all individuals with SFK.
• Lifestyle modifications including diet, physical activity, and avoidance of nephrotoxins are critical.
• Early detection of albuminuria, hypertension, and decreased GFR allows for timely interventions to preserve renal mass.