[SOLITARY KIDNEY - IS IT TOO LITTLE?]

INTRODUCTION: Solitary functioning kidney (SFK) occurs with unilateral renal agenesis (URA) in 1/2000 live births - or after uninephrectomy for tumor, trauma, uncontrolled infections or hypertension and post-kidney donation. URA-associated states include urological, cardiac, gastrointestinal and skeletal anomalies or it might be a component of a genetic syndrome. In 10% of cases of URA another family member is affected. In any case of SFK a compensatory process is triggered consisting of glomerular hypertension with hyperfiltration which achieves 75% of two kidneys' function. In the long-run this process might be detrimental causing further loss of functioning nephrons, inability to sustain functional compensation and progressive kidney function deterioration. The risk for this chain of events is determined in the first place by the number of nephrons in the SFK, which cannot be assessed in vivo. Hints for reduced nephron number in the single kidney include prematurity or SGA-small for date birth weight, urological anomalies with or without accompanying infections, lack of increased single kidney size - compensatory hypertrophy. Age of onset of the compensatory process and acquired factors including nephrotoxin exposure, overweight/obesity, excessive salt and/or protein intake contribute to the risk of progressive renal damage. Life-long follow-up of all subjects with SFK is recommended from early age for lifestyle education: recommended diet and tailored physical activity, nephrotoxin avoidance along with early detection of renal injury signs: albuminuria, hypertension or depressed kidney function - GFR (glomerular filtration rate) targeting timely intervention for preservation of functioning renal mass.