Why Check Renal Function in Patients with Small for Gestational Age (SGA) History
Renal function monitoring is essential in individuals born SGA because they have reduced nephron numbers, impaired kidney development, and demonstrable renal dysfunction that begins in early childhood and persists into adulthood, placing them at increased risk for chronic kidney disease and hypertension.
Evidence of Renal Impairment in SGA Individuals
Early Childhood Findings (Preschool Age)
Children born SGA demonstrate altered renal tubular function by age 5 years, including increased urinary calcium excretion (calcium-creatinine ratio 0.16 ± 0.08 in SGA vs 0.10 ± 0.09 in controls, p=0.04) and decreased uric acid excretion despite elevated serum uric acid levels (fractional excretion 7.4% ± 4% in SGA vs 10.5% ± 5.9% in controls, p=0.02) 1.
Blood pressure elevation correlates with severity of growth restriction, with systolic BP reaching 107.5 ± 11 mmHg in SGA children with birth weight <3rd percentile versus 102 ± 10 mmHg in controls (p=0.03) by preschool age 1.
Kidney size remains smaller in preterm SGA infants (<36 weeks gestational age) with impaired relative kidney length persisting through the second year of life, indicating inadequate compensatory growth 2.
Mid-Childhood Findings (Age 11 Years)
Estimated GFR progressively decreases from term AGA children through preterm AGA to preterm SGA children, with the most severe impairment in those born both extremely preterm and SGA 3.
Plasma symmetric dimethyl arginine (SDMA) levels increase progressively in the same pattern (term AGA < preterm AGA < preterm SGA), providing an independent marker of renal dysfunction 3.
Children born extremely preterm (<28 weeks) or extremely low birth weight (<1000g), particularly those also born SGA, demonstrate measurable renal function impairment by age 11 years across multiple validated estimation equations 3.
Young Adult Findings (Age 20 Years)
Effective renal plasma flow (ERPF) is significantly reduced in young adults born preterm and SGA, measuring 71 mL/min/1.73 m² less than controls (95% CI: 3-139) even after body surface area adjustment 4.
Kidney length and volume remain significantly smaller in adults born preterm and SGA compared to term-born controls, with renal function correlating directly with renal size 4.
Microalbuminuria is present in 8.7% of young adults born preterm and SGA versus 0% in controls, indicating early glomerular damage 4.
Pathophysiologic Mechanisms
Developmental Alterations
Intrauterine growth restriction causes reduced nephron endowment during the critical period of nephrogenesis, which is complete by 36 weeks gestation, resulting in permanent nephron deficit 2, 1, 4.
Preterm birth compounds the problem by interrupting normal kidney development, with the most severe effects in infants born <36 weeks gestational age who show persistently impaired relative kidney length 2.
Compensatory kidney growth patterns differ by gestational age: full-term SGA infants demonstrate catch-up kidney growth by 3 months of age, while preterm SGA infants (<36 weeks) fail to achieve normal relative kidney length through 24 months 2, 5.
Progressive Nature of Renal Dysfunction
Renal impairment is demonstrable across the lifespan, beginning with tubular dysfunction in preschool years, progressing to reduced GFR in mid-childhood, and persisting with decreased ERPF and microalbuminuria in young adulthood 1, 4, 3.
The severity of renal dysfunction correlates with the degree of growth restriction at birth, with those born <3rd percentile showing more severe impairment than those born between 3rd-10th percentile 2, 1.
Clinical Monitoring Recommendations
Baseline Assessment
Measure serum creatinine and calculate estimated GFR using validated pediatric equations (Schwartz, Zappitelli, or Gao formulas depending on age) 3.
Obtain plasma cystatin C and SDMA levels as additional markers of renal function that are less dependent on muscle mass 3.
Perform renal ultrasonography to measure kidney length and volume, as renal size correlates with function and identifies those with inadequate compensatory growth 2, 4, 5.
Functional Assessment
Collect timed urine specimens (3-hour collections are adequate) to calculate urinary albumin excretion, fractional excretion of sodium, potassium, phosphate, magnesium, and uric acid, and urinary calcium-creatinine ratio 1.
Measure blood pressure at every visit, as hypertension develops early and correlates with severity of growth restriction 1, 3.
Monitor serum uric acid levels alongside fractional excretion of uric acid, as SGA children demonstrate impaired uric acid handling 1.
Timing of Surveillance
Begin screening in preschool years (age 5) when tubular dysfunction and blood pressure elevation first become evident 1.
Repeat comprehensive assessment at age 11 years when GFR reduction and SDMA elevation are consistently demonstrable 3.
Continue monitoring into young adulthood as microalbuminuria and reduced ERPF persist, indicating ongoing risk for chronic kidney disease 4.
Common Pitfalls to Avoid
Do not assume normal serum creatinine excludes renal dysfunction in SGA individuals, as tubular dysfunction and reduced ERPF may precede GFR decline; use multiple markers including cystatin C, SDMA, and urinary studies 1, 4, 3.
Do not rely on kidney size alone to assess renal function, as some full-term SGA infants achieve normal kidney length despite persistent functional abnormalities 5.
Do not overlook the combined effect of prematurity and SGA status, as those born both preterm (<36 weeks) and SGA have the most severe and persistent renal impairment 2, 4, 3.
Do not delay screening until symptoms develop, as renal dysfunction is demonstrable in asymptomatic children and early identification allows for risk factor modification 1, 3.