PROTEINURIA, HEMATURIA, AND SERUM CREATININE CORRELATE WITH THE PATHOLOGICAL SEVERITY INDEX IN PATIENTS WITH GLOMERULONEPHRITIS (LONGITUDINAL STUDY: DEVELOPMENT OF A CLINICAL-PATHOLOGICAL SCORING SYSTEM IN GLOMERULONEPHRITIS PATIENTS)

The incidence of Chronic Kidney Disease (CKD) is rising annually, both in Indonesia and globally. The incidence is not only rising but is also associated with morbidity, mortality, and chronic complications. The current classification of chronic kidney disease (CKD) is determined not only by estimated glomerular filtration rate (eGFR) but also considers the level of albuminuria and its etiology. The etiology of chronic kidney disease (CKD), frequently undiagnosed and associated with a poor prognosis, is glomerulonephritis (GN). The diagnosis of GN requires confirmation through biopsy, evaluating both morphological and immune activity characteristics. Additional prognostic evaluation necessitates scoring, which is applicable solely to specific types of glomerulonephritis (GN). The correlation between the levels of activity and chronicity in the glomeruli, tubules, and interstitium, alongside various pertinent routine clinical markers like proteinuria and hematuria, remains controversial. Consequently, it is essential to undertake additional research to establish a scoring system applicable to all GN spectrums and its correlation with these standard clinical markers. The purpose of this study was to determine the relationship between the pathological severity index (PSI) score and proteinuria, hematuria, and SC in GN patients.

We conducted a longitudinal observational study from 2016 to 2024 at RSUP Prof. Dr. I.G.N.G. Ngoerah. We included patients aged 12–65 years who underwent native-kidney biopsy with ≥4 glomeruli; we excluded cases with incomplete records, diabetes mellitus, or allograft biopsies. Proteinuria was assessed semi-quantitatively by urine dipstick and hematuria by urine-sediment red blood cell counts; pre-biopsy values were analyzed. The PSI was a semi-quantitative histopathological score summing four compartmental indices—glomerular, tubular, interstitial, and vascular—each comprising abnormality, activity, severity, and distribution sub-scores where applicable. In brief, glomerular severity was graded 0–3 (0 normal; 1 cellular crescent; 2 fibrocellular crescent; 3 fibrous crescent/fibrosis/sclerosis) and distribution 0–2 (0 normal; 1 focal; 2 diffuse). Tubular abnormalities (0/1), activity (0–2, from early injury to atrophy), and distribution (0–2) were recorded; interstitial abnormalities (0/1), activity (0–3, from cellular infiltration to fibrosis), and distribution (0–2) were recorded; vascular abnormalities (0/1) and activity (0–2, from endothelial injury to fibrosis/sclerosis) were recorded. We used descriptive statistics, the one-sample Kolmogorov–Smirnov test for normality, Pearson/Spearman correlations, and multivariable linear regression (backward selection); significance was set at p<0.05. Analyses were performed in IBM SPSS for Mac version 29.

We included 150 participants (mean age 28.37±12.22 years). Biopsy cores contained a mean of 20.29±10.58 glomeruli. Post-biopsy diagnoses were lupus nephritis (n=58), focal segmental glomerulosclerosis (FSGS; 19.3%, n=29), IgA nephropathy (11.3%, n=17), minimal change disease (10.7%, n=16), membranoproliferative GN (MPGN; 6.7%, n=10), membranous nephropathy (2.7%, n=4), and other diagnoses (3%). The mean PSI was 10.13±4.56 (glomerular index 4.49±2.32; tubular 2.90±1.56; interstitial 2.36±1.78; vascular 0.41±0.88). PSI correlated positively with proteinuria (r=0.299; p<0.01), PCR (r=0.204; p=0.038), hematuria (r=0.168; p=0.04), and SC (r=0.255; p=0.002). In multivariable analysis (backward model), only proteinuria and SC independently predicted PSI (PSI = 7.57 + 0.845×[proteinuria—urinalysis] + 0.471×SC), with adjusted R²=0.116 (p<0.01).

Among patients with GN, higher PSI scores were associated with greater proteinuria, hematuria, and higher SC.