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Acute post-streptococcal glomerulonephritis (APSGN) typically presents with hematuria, edema, and hypertension. Although short-term outcomes are generally favorable, several long-term studies have reported that a subset of patients later develop hypertension, proteinuria, or renal dysfunction, suggesting that prognosis is not uniformly benign. APSGN remains one of the most common causes of acute glomerulonephritis in children worldwide, yet imaging-based evaluation of subtle renal microstructural changes has been limited.
We report the case of a previously healthy 9‑year‑old boy, with no family history of renal disease and normal prior school urinalysis, who presented with headache, nausea, and edema but no gross hematuria. On admission, he had generalized edema and hypertension. Laboratory tests showed hypocomplementemia (low C3, normal C4) and elevated antistreptolysin O titer, while urinalysis remained normal. Throat culture was positive for group A streptococcus. Renal biopsy revealed diffuse endocapillary hypercellularity with neutrophil infiltration, subepithelial humps, and granular IgG/C3 deposition, with additional positivity for nephritis‑associated plasmin receptor and plasmin, consistent with APSGN. This case highlights extrarenal‑symptomatic APSGN confirmed by biopsy.
Renal magnetic resonance imaging was performed on a 1.5‑T scanner at four time points: baseline (at biopsy), 2 weeks, 6 months, and 1 year. Diffusion tensor imaging (DTI) parameters—mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD)—were quantified in cortical and medullary regions using manually placed regions of interest. Because the biopsy was performed on the right kidney, DTI parameters were consistently measured in the left kidney to avoid procedure‑related artifacts. DTI metrics were processed and calculated using DSI Studio (http://dsi-studio.labsolver.org), ensuring reproducibility of parameter estimation. Serum creatinine‑based estimated glomerular filtration rate (eGFR) and complement C3 were measured concurrently. Statistical analysis was performed with the Friedman test and Dunn’s post‑hoc correction.
eGFR and complement C3 normalized by 6 months and remained stable thereafter, while urinalysis was consistently normal. In contrast, medullary DTI parameters exhibited a biphasic course: MD, AD, and RD were elevated at baseline, decreased below baseline at 6 months, and increased again at 1 year, whereas cortical parameters showed only mild, transient alterations. Medullary results are summarized in Table 1, which integrates clinical (eGFR, C3) and imaging (MD, AD, RD) parameters. These biphasic changes were statistically significant compared with baseline values.
Table 1. Longitudinal changes in renal function, complement C3, and medullary DTI parameters (MD, AD, RD)
*Values are mean ± SD. eGFR and complement C3 normalized by 6 months. Cortical parameters showed only mild, transient alterations and are not shown. Statistical analysis: Friedman test with Dunn’s correction. ns, not significant; *p < 0.05; *p < 0.01; ****p < 0.0001 vs baseline.
This case demonstrates that, despite complete clinical recovery and normalization of laboratory parameters, medullary DTI parameters followed a biphasic trajectory. Previous reports suggest that APSGN may predispose to hypertension, proteinuria, or renal dysfunction decades after onset, indicating that long‑term outcomes are not uniformly benign. Our findings suggest that DTI may serve as a sensitive biomarker for detecting subclinical renal alterations, bridging the gap between short‑term recovery and long‑term risk. Further longitudinal studies are warranted to determine whether such imaging changes predict adverse outcomes in later life. In particular, alterations in MD, AD, and RD may reflect distinct aspects of renal microstructural integrity—overall diffusivity, tubular directionality, and membrane‑related barriers—indicating that DTI could provide mechanistic insights beyond conventional clinical markers.