ABSTRACT
Membranous nephropathy is a common cause of nephrotic syndrome in adults. It usually occurs secondary to underlying disease processes such as autoimmune disorders, malignancy, infection, and drugs. The presentation of nephrotic syndrome with concomitant precipitous decline in renal function warrants investigation of a coexistent disorder.We report the case of a 30-year-old male who presented with symptoms and signs of hypothyroidism.A diagnosis of Hashimoto's thyroiditis was contemplated based on the presence of high serum levels of antithyroglobulin and antithyroid peroxidase antibodies. Upon initiation of treatment with levothyroxine, patient symptomatology improved; however, the laboratory studies demonstrated continued elevated creatinine, hematuria, and proteinuria, which had not been addressed. Two months following treatment initiation, he had progressive deterioration in renal function and proteinuria. A renal biopsy revealed coexistent necrotizing and crescentic glomerulonephritis and membranous nephropathy.The final diagnosis was necrotizing, crescentic glomerulonephritis with superimposed membranous nephropathy likely secondary to Hashimoto's thyrodiitis.Induction treatment with oral cyclophosphamide and prednisone was started.At the end of 6 months of treatment, there was improvement in renal function and proteinuria and maintenance treatment with azathioprine and low-dose prednisone was initiated. This case highlights the importance of precise and detailed evaluation of patients with autoimmune diseases such as Hashimoto's thyroiditis particularly in the presence of active urine sediment. Proper evaluation and diagnosis of such patients has implications on the prognosis and response to treatment.
Subject(s)
Glomerulonephritis, Membranous/pathology , Hashimoto Disease/complications , Adult , Azathioprine/therapeutic use , Cyclophosphamide/therapeutic use , Glomerulonephritis/etiology , Glomerulonephritis, Membranous/drug therapy , Hashimoto Disease/drug therapy , Humans , Male , Prednisolone/therapeutic use , Thyroxine/therapeutic useABSTRACT
Immigrants attempting to cross the border often wander for days without food or water, subsequently developing acute kidney injury (AKI) secondary to rhabdomyolysis. In this article, we describe our experience with myoglobinuric AKI in these border crossers. Records from all patients in the custody of the border patrol from 1 June 2010 to 30 June 2011, who had AKI defined by the Acute Kidney Injury Network (AKIN) criteria and a CK > 1000 IU/L, were reviewed. The age, gender, temperature, days in the desert, initial serum creatinine, CK on presentation, need for dialysis, length of hospital stay, and serum creatinine at discharge were recorded and analyzed. Forty-two patients developed myoglobinuric AKI with a mean age of 32.5 years. Among them, 38 were males and four females. There was a mean of 4.2 days in the desert. Seven had stage 1 AKI, 10 stage 2, and 25 stage 3. 5 patients required hemodialysis. Only one patient had a temperature >100.6ºF on arrival. CKs ranged between 1101 and 447,966 IU/L. Mean length of stay was 4 days. Two patients were discharged on hemodialysis and eight were discharged with serum creatinine levels of >1.3 mg/dL. This is the largest series of myoglobinuric AKI reported in border crossers. The kidney injury is presumably due to the excessive heat combined with volume depletion. We have coined the term "border crossers' nephropathy" for this disorder. This is a serious problem that has both political and economic consequences on both sides of the border.
