CRESCENTIC GLOMERULONEPHRITIS ASSOCIATED TO INFECTIVE ENDOCARDITIS

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CRESCENTIC GLOMERULONEPHRITIS ASSOCIATED TO INFECTIVE ENDOCARDITIS
Sebastián
Gortari
Gabriela Ottati gottati@gmail.com Hospital Policial Nephrology Montevideo
Diego Tobal dtobal@gmail.com Hospital Policial Nephrology Montevideo
Jacqueline Nalerio jacquelinenalerio@gmail.com Hospital Policial Nephrology Montevideo
Alejandra Ferrari Aferrari@gmail.com Hospital Policial Nephrology Montevideo
Andrés Urrestarazu docurre@gmail.com Hospital Policial Nephrology Montevideo
Ruben Coitiño rucoitino@gmail.com Hospital Policial Nephrology Montevideo
Maria Aunchayna mhaunchayna@hotmail.com Hospital de Clinicas Pathology Montevideo
 
 
 
 
 
 
 
 

The following clinical case is a glomerulonephritis (GN) suspected to be related to infectious endocarditis with negative blood cultures, posing a diagnostic and therapeutic challenge.

47 years old male patient, with no prior history of kidney disease ( creatininemia 1.1 mg/dl and urine examination without  proteinuria or microhematuria 09/2022), presenting fever, edema of the lower extremities, hypertension, vasculitis lesions on the ankles, and splinter hemorrhages on the toes. Simultaneously, he presents oliguria, macrohematuria, and foamy urine. Three weeks before, he presented acute pharyngitis.

 

Physical examination at admission: Temperature 38.5°C, blood pressure 160/90 mmHg. Dental septic foci. Congested pharynx. Petechiae on both ankles. Splinter hemorrhages on both hands. Regular rhythm at 110 beats per minute, no murmurs or pericardial rub. Edema of lower extremities up to the knees, bilateral and symmetrical. No jugular engorgement or hepatojugular reflux. The rest of the physical examination showed no significant findings.

 

Lab findings:

Anti-streptolysin O (ASLO) 297 IU/ml (reference range <200).

C-Reactive Protein 205 mg/l, Erythrocyte sedimentation rate 130 mm/h.

Creatinine 2.1 mg/dl, Azotemia 1.43 g/l.

Urinalysis: White blood cells 5-12/HPF, abundant red blood cells/HPF. Proteinuria 3.2 g/day.

Complement: C3: 155 (reference range 90-180), C4: 36 (reference range 10-40).

Rheumatoid factor 12 IU/ml (reference range <10).

Transthoracic Echocardiogram: An oscillating intracardiac mass on the Aortic Valve, compatible with a small vegetation.

ANCA negative, ANA negative, Blood culture negative, Hepatitis panel negative.

 

Given the diagnosis of Nephritic syndrome a kidney biopsy was performed. Renal corticomedullary sample, eleven glomeruli, one of which shows global sclerosis. The remaining glomeruli exhibit the following features: increased cellularity with mesangial and segmental endocapillary cellularity in more than 50% of the glomeruli, as well as cellular and fibrocellular proliferation in three glomeruli. Crescent formations are present, occupying up to 20% of the glomerular circumference. There is glomerulitis and glomerular necrosis. The capillary basement membranes are thin. With the trichrome stain, pericapillary deposits are observed in subepithelial locations. The interstitium displays diffuse fibrosis (15%) with a lymphomonocytic inflammatory infiltrate and scattered polymorphonuclear neutrophils (PMN). Immunopathological examination shows intense granular deposits of IgG and C3, as well as moderate deposits of light chains (Kappa and Lambda). Absence of IgA, IgM, C1q, and Fibrinogen. In summary, Diffuse proliferative glomerulonephritis with immune deposits, consistent with post-infectious glomerulonephritis.Results

Crescentic GlomerulonephritisThe patient received antibiotics, and concomitantly, intravenous pulses of Methylprednisolone, followed by oral Prednisone. He has shown good clinical improvement, disappearance of macrohematuria progressive decrease in creatininemia and proteinuria.

In this clinical case the diagnostic challenges arose from the absence of positive blood cultures in a probable infective endocarditis with renal involvement, highlighting the importance of alternative diagnostic methods such as renal biopsy. The concomitance of IgG and C3, the presence of PMN and the favorable evolution of the clinical picture tip the balance towards the diagnosis of GN linked to infection.

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