Background: Lupus podocytopathy (LP) is a non-immune complex-mediated glomerular lesion in systemic lupus erythematosus (SLE), characterized by the diffuse effacement of podocyte processes without immune complex deposition or with only mesangial immune complex deposition. LP is a rare cause of nephrotic syndrome in SLE patients with implications for prognosis and treatment. Case Report: We present the case of a 28-year-old woman with a medical history of type 1 diabetes mellitus (T1DM) who presented with lower limb edema, dyspnea, hypercholesterolemia, with nephrotic range proteinuria, without acute kidney injury, and laboratory findings compatible with auto-immune hemolytic anemia. They had negative infectious serology, positive antinuclear antibody (ANA), and an eye fundus examination showing diabetic retinopathy. A biopsy was performed to define the etiology of the renal involvement, which was compatible with LP. Following immuno-suppressive and antiproteinuric therapy, the patient evolved with the complete remission of the nephrotic syndrome. Conclusions: Lupus podocytopathy is an infrequent anatomopathological entity, so this case is presented as the first reported in Peru, and a literature review is made.

Background/Objectives: Acetazolamide is widely used for acute mountain sickness (AMS) prophylaxis. Whilst generally safe, acute kidney injury (AKI) is a rare but serious adverse event. We present a case of anuric AKI following minimal exposure to acetazolamide, contributing to the limited literature on its nephrotoxicity at prophylactic doses. Methods: A 54-year-old previously healthy male ingested 250 mg/day of oral acetazolamide for two days. He developed acute anuria and lumbar pain. Diagnostic evaluation included laboratory tests, imaging, microbiological cultures, autoimmune panels, and diuretic response. No signs of infection, urinary tract obstruction, or systemic disease were found. Results: The patient met KDIGO 2012 criteria for stage 3 AKI, with peak serum creatinine of 10.6 mg/dL and metabolic acidosis. Imaging confirmed non-obstructive nephrolithiasis. Conservative treatment failed; intermittent hemodialysis was initiated. Renal function recovered rapidly, with the normalization of serum creatinine and urinary output by day 4. Conclusions: This case represents the lowest cumulative dose of acetazolamide reported to cause stage 3 AKI. The findings support a pathophysiological mechanism involving sulfonamide-induced crystalluria and intratubular obstruction. Physicians should consider acetazolamide in the differential diagnosis of AKI, even with short-term prophylactic use.