EPIDEMIOLOGY,CLINICAL ,PATHOLOGICAL PROFILE ,LABORATORY AND HISTOLOGICAL PARAMETERS IN INFECTION RELATED GLOMERULONEPHRITIS

 

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EPIDEMIOLOGY,CLINICAL ,PATHOLOGICAL PROFILE ,LABORATORY AND HISTOLOGICAL PARAMETERS IN INFECTION RELATED GLOMERULONEPHRITIS

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Dr PAPAIAH NIRMAL
PUDOTA
Dr PAPAIAH NIRMAL PUDOTA pudotanirmal@gmail.com Krishna institute of medical sciences Nephrology Hyderabad India *
Dr ASWINI DUTT TRIPURANENI aswinidutt10@gmail.com Krishna institute of medical sciences Nephrology Hyderabad India -
Dr VS REDDY vsreddykims@gmail.com Krishna institute of medical sciences Nephrology Hyderabad India -
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Infection-related glomerulonephritis (IRGN) is an immune complex-mediated acute glomerulonephritis involving both in situ and circulating immune complexes in association with a variety of non-renal infections.There has been a dramatic shift in the epidemiology of IRGN over the past few decades. Adult IRGN is associated with a wider spectrum of non-streptococcal agents, especially staphylococcal and Gram-negative organisms.It can be associated with a more heterogeneous set of infectious sites (beyond skin and upper respiratory tract), with few of them even harbouring infection at more than one site.IRGN without an apparent infectious focus can be associated with occult visceral or deep-seated abscess-making it imperative that there should be an extensive search for any occult primary source of infection. Aggressive measures to eradicate active infection are warranted to salvage the renal function. We did a prospective study of biopsy-proven adults with IRGN to analyse the clinicopathological profile, outcome and predictors of prognosis.

This prospective observational study was done at Muthya Kidney Centre   ,Warangal ,Telangana,India from April 2024 to August 2025 .All patients aged >12 years with a definitive diagnosis of IRGN were enrolled. As no single clinical or pathological finding is pathognomic for IRGN, the diagnosis was based on the criteria for IRGN .

At least three of the following five criteria are required: (i) clinical or laboratory evidence of infection preceding or at the onset of glomerulonephritis; (ii) depressed serum complement; (iii) endocapillary proliferative and exudative glomerulonephritis; (iv) C3-dominant or co-dominant glomerular immunofluorescence staining; and (v) hump-shaped sub-epithelial deposits on electron microscopy (EM). Those with HIV and hepatitis B or C infection were excluded. IgA-dominant IRGN patients were included. History, physical examination and laboratory investigation findings were documented. The presence of underlying comorbid conditions such as diabetes mellitus, alcoholism, malignancy, immunosuppressive intake, cirrhosis, HIV seropositivity, intravenous drug abuse and severe malnutrition was noted.


All patients had the following investigations: complete blood count with peripheral smear, urine analysis; urine protein–creatinine ratio (uPCR); blood sugar; blood urea; serum creatinine; serum electrolytes; liver function tests; serum albumin; serological tests for HIV, hepatitis B and hepatitis C; complement levels (C3 and C4); antistreptolysin O titre and C-reactive protein levels. Antinuclear antibody (ANA) and antineutrophil cytoplasmic antibodies (ANCA) were done in selected patients.


Kidney biopsy was done in all patients under ultrasound guidance using the Bard Max-core disposable core biopsy instrument. Tissue samples were studied under light microscopy with haematoxylin and eosin, periodic acid–Schiff, Jone’s methena-mine silver and Masson’s trichrome stains. Immuno-fluorescence (IF) staining was performed on 3-μm cryostat sections using polyclonal fluorescein-isothiocyanate-conjugated antibodies to IgG, IgM, IgA, C3, C1q, C4, kappa and lambda light chains. The intensity of IF staining was graded on a scale of 0–3. All the biopsy samples were reported by the same renal pathologist.


All patients were followed up, and the following parameters were recorded in the subsequent visits: blood pressure, uPCR, urine sediments and serum creatinine. C3 and C4 levels beyond 3 months of presentation were done in every patient.


Statistical analysis


Univariate analysis of categorical variables was done using the chi-square test. Statistical significance was assumed at p<0.05. Statistical analysis was done using MedCalc statistical software. Predictors of failure to achieve complete recovery were identified by logistic regression analysis.


25 Patients were studied with a mean (SD)follow up of one

The mean age was 36 years (18-70) years with a  male preponderance (4:1.)

Majority of the patients had nephritic syndrome at presentation  

30% of the patients had diabetes and hypertension as comorbidities 

Around 60% of the patients were hypertensive with pedal Edema in 60% and gross or microscopic hematuria in 50-60%

 And oliguria in 10%

 1-2 patients required dialysis due to rapidly progressive renal failure presentation.

Hypocomplementemia was present in almost 96% of patients 

Salient Pathological features were endo capillary proliferation (98.7%),Neutrophilic infiltratation (95.3%)

Presence of crescents (10.2%).Interstitial inflammation (40-50%) with mild to moderate IFTA (20%)

90% of the patients had complete recovery 

By logistic regression analysis, the predictors of Poor outcome were a requirement for dialysis at presentation (p=0.04) and presence of IFTA (p = 0.03).


Infection -Source of infection was identified 

Skin and soft tissue -50-60%

Lung -10%

Urinary tract -30%

Patients  with nephrotic range proteinuria and crescents were given oral steroids for a period of 4-6 weeks with 0.5mg/Kg dose and majority had responded with complete remission 

Time for remission was prolonged with those with Acute kidney injury and nephrotic range proteinuria with a median duration of 1-2 months 


Male female 
196
73%27%

       

Epidemiology Male to female Ratio 


Syndromic Presentation 



Histopathological sub type or variant in IRGN


Blood pressure 





Nephrotic syndrome   9      36%
Nephritic syndrome 1352%
RPRF   3       
12%    
  
Comorbidities  

Diabetes 36%
Hypertension 
20%



  
C3 low low c3.  and c4 
96%4%

Infection-related glomerulonephritis (IRGN) is associated with glomerular immune complex deposition along with complement activation with More male to female ratio presentation Steroids may attenuate glomerular injury and thereby improve renal outcomes especially those with nephrotic range proteinuria and presence of crescents.Infection related glomerulonephritis carries a favourable prognosis and only less than 5% of patients in our study progressed further over the months .Adult associated IRGN is commonly seen in our study compared to PIGN .Majority of patients in our study had c3 and iGg associated IRGN with 20% of patients having combined diabetic Nephropathy with infection associated glomerulonephritis. 

Kewords