Endocrine Abstracts

Background: The commonest etiology for the chronic kidney disease and end-stage renal disease, universally, is diabetes. Although, the histology of the kidney is the gold standard for diagnosing diabetic kidney disease, but in common practice it’s usually diagnosed clinically and through laboratory testing.

Clinical Case: 43 yrs old Saudi house-wife was admitted on the 7th of February, 2024 with 5 months history of progressive pitting pedal edema, facial puffiness, followed by dyspnea (NYHA-III), orthopnea, paroxysmal nocturnal dyspnea and frothy urine for 1 month, prior to the admission. She had a past medical history of long-term Type 2 diabetes and Chronic liver disease (HBV+). Systemic review-weight gain and anorexia. Family history unremarkable. No allergies or addictions. She also developed acute diarrhea during the admission. On evaluation, the patient was found to have the following issues: 1-Diabetic kidney disease (anasarca with moderate ascites+, hypoalbuminemia [S.albumin 26 (39.7-49.4 g/l)], S. Creatinine 140(45-84umol/l), Albuminuria (Albumin/Creatinine-2541(0-30 mg/g), CBC (Hb% 95(12-16 g/l, MCV 86.6fl, TLC and PLTs normal), HbA1c 8.7%, US abdomen (normal liver, spleen, portal vein & kidneys, moderate ascites and right pleural effusion), ascitic tap (serum-ascitic albumin gradient 0.8 g/l) and renal biopsy showed Class III DM nephropathy (classification 2010), with secondary focal segmental glomerulosclerosis 2- Right renal vein thrombosis with poor right renal perfusion (US proven) 3- Clostridium-difficile colitis (toxin+on stool testing. Other important investigations- Hepatitis B core and e Abs +, HBV PCR 159 IU/ml, Auto-immune workup negative. Serum immune electrophoresis-polyclonal gammopathy, Transthoracic Echo-mild concentric left ventricular hypertrophy with normal LV systolic function, moderate pericardial and left pleural effusions, US pelvis-anterior sub-serosal fibroid (2.7 × 2.9 cms)

Results: The patient was managed with moderate protein intake, diuretics, oxygen, fluid restriction, therapeutic abdominal paracentesis, apixaban,, angiotensin receptor and calcium channel blockers, atorvastatin, dapagliflozin, linagliptin and basal-bolus insulin. Her condition got stabilized and was advised follow-ups in the nephrology, hepatology and gynecology clinics.

Conclusions: Our case taught us that one should never assume the heavy proteinuria in diabetes to be related to diabetic nephropathy, until the secondary causes have been excluded. The value of the tissue biopsy in arriving at the precise diagnosis, cannot be overemphasized.