Systemic Lupus Erythematosus in the Elderly That Debuts With an Organic Manifestation of Lupus Nephritis.

Systemic lupus erythematosus (SLE) is a systemic autoimmune condition with many clinical presentations. It is classically seen in young to middle-aged females and can present with cutaneous, renal, serosal, hematological, joint, and/or neurological manifestations at the time of diagnosis or may develop over the course of the disease. Late-onset SLE or SLE in the elderly is a subtype that differs from the classic SLE in age group, clinical presentation, involvement of organs, and severity. Here, we present the case of a geriatric Hispanic male noted to have worsening renal function. The patient was diagnosed with lupus nephritis (LN) upon obtaining serological markers and renal biopsy. LN, a renal sequela of SLE, presents with a full-house immunofluorescence pattern. LN, along with high titers of the antinuclear antibody (ANA) and/or anti-double-stranded DNA (anti-dsDNA) antibody, is an effective tool to diagnose SLE in patients without extrarenal manifestations of the disease. The patient was managed with glucocorticoids and mycophenolate mofetil therapy, which led to a rapid downtrend of creatinine, resulting in stabilization of renal function and deferring the need for a hemodialysis. This case highlights the topic of late-onset SLE presenting with LN in geriatric patients.

Acute oxalate nephropathy associated with orlistat.

BACKGROUND: Obesity is a major world-wide epidemic which has led to a surge of various weight loss-inducing medical or surgical treatments. Orlistat is a gastrointestinal lipase inhibitor used as an adjunct treatment of obesity and type 2 diabetes mellitus to induce clinically significant weight loss via fat malabsorption. CASE PRESENTATION: We describe a case of a 76-year-old female with past medical history of chronic kidney disease (baseline serum creatinine was 1.5-2.5 mg/dL), hypertension, gout and psoriatic arthritis, who was admitted for evaluation of elevated creatinine, peaking at 5.40 mg/dL. She was started on orlistat 120 mg three times a day six weeks earlier. Initial serologic work-up remained unremarkable. Percutaneous kidney biopsy revealed massive calcium oxalate crystal depositions with acute tubular necrosis and interstitial inflammation. Serum oxalate level returned elevated at 45 mm/l (normal <27). Timed 24-hour urine collection documented increased oxalate excretion repeatedly (54-96 mg/24 hour). After five renal dialysis sessions in eighth days she gradually regained her former baseline kidney function with creatinine around 2 mg/dL. Given coexisting proton-pump inhibitor therapy, only per os calcium-citrate provided effective intestinal oxalate chelation to control hyperoxaluria. CONCLUSIONS: Our case underscores the potential of medically induced fat malabsorption to lead to an excessive oxalate absorption and acute kidney injury (AKI), especially in subjects with pre-existing renal impairment. Further, it emphasizes the importance of kidney biopsy to facilitate early diagnosis and treatment.

Kidney biopsy for renal tubular acidosis: when tissue diagnosis makes a difference.

Renal tubular acidosis (RTA) is a disorder with variable presentations and oftentimes a nebulous underlying primary diagnosis. We describe a rare cause of RTA as an unusual complication of proton pump inhibitor (PPI) therapy. We report a case of a 33-year-old male with history of hypertension, acid reflux, allergic rhinitis, and low testosterone admitted with complaints of fatigue, weight loss, and unexplained acidosis for ~ 2 months. His medications prior to admission included losartan, omeprazole, potassium chloride, sildenafil, and testosterone propionate injections. His physical exam was unremarkable with a blood pressure of 120/80 mmHg. Initial lab work showed a nonanion gap metabolic acidosis with serum bicarbonate level of 16 mM/L and potassium 3 mM/L. Urine studies showed urine pH of 6.5 and a positive urine anion gap. The serum creatinine was within normal range(1.13 mg/dL). He required massive doses of bicarbonate and potassium supplementation with minimal improvement of serum chemistries achieved. The cause of apparent distal RTA remained elusive despite extensive blood, urine, and imaging testing. Ultimately a renal biopsy was obtained showing mild to moderate tubule-interstitial inflammation with 5% fibrosis. PPI therapy (omeprazole) was stopped, and he was started on prednisone 60 mg per day. Two weeks later, his RTA findings resolved, and he no longer required bicarbonate and potassium supplementation. Our case highlights the importance of recognizing a unique complication of RTA following PPI therapy. It also underscores the possible need for considering a kidney biopsy in the setting of nondiagnostic laboratory work up to uncover the underlying etiology of RTA and suspected allergic interstitial nephritis (AIN).

Granulomatous interstitial nephritis associated with disseminated histoplasmosis in an immunocompetent patient.

We present a case of a 64-year-old man with a prolonged history of fatigue, weight loss, fever, and kidney failure. Kidney biopsy showed severe granulomatous interstitial nephritis with numerous giant cells. Silver stains identified fungal micro-organisms consistent with Histoplasma species. Despite antifungal treatment, the patient died of overwhelming infection a few weeks later. This report emphasizes the importance of diagnosing histoplasmosis early. A high degree of suspicion is required to make the diagnosis of histoplasmosis in a case of granulomatous interstitial nephritis.