Yeong-Hau H. Lien

Long-term cyclophosphamide treatment for recurrent type I membranoproliferative glomerulonephritis after transplantation

The incidence of recurrent type I membranoproliferative glomerulonephritis (MPGN) after renal transplant is approximately 30%, and the rate of graft loss due to recurrent MPGN type I is higher than 50%. The treatment of this disease has not been defined. We report a case of recurrent MPGN type diagnosed 4 months after a cadaveric renal transplantation. The patient was treated with cyclophosphamide and was able to maintain her graft function. Cyclophosphamide was interrupted three times during the course. Each time her renal function deteriorated and her serum albumin decreased. The patient currently has a functional renal graft 3 years after transplantation while receiving low-dose therapy with cyclophosphamide. We suggest treating recurrent type I MPGN with cyclophosphamide while continuing the calcineurin inhibitor and prednisone.

Ciprofloxacin-induced granulomatous interstitial nephritis and localized elastolysis

Ciprofloxacin is known to cause acute interstitial nephritis. We report the first case of ciprofloxacin-induced granulomatous interstitial nephritis and localized elastolysis. The patient presented with acute renal failure and skin lesions following a 14-day course of ciprofloxacin administered for cellulitis. The patient had symmetric, palm-sized, tender violaceous plaques on both axillae. The renal biopsy revealed granulomatous interstitial disease. A skin biopsy revealed an elastolytic process with histocytic infiltration and calcification. After discontinuing ciprofloxacin and starting a short course of steroid therapy, the skin lesion and renal function improved promptly. The nephritis relapsed after prednisone was discontinued and responded to a second course of steroid therapy. Ciprofloxacin, like penicillin, can cause granulomatous interstitial nephritis and elastolysis. A prolonged course of steroid therapy may be indicated in patients with ciprofloxacin-induced granulomatous interstitial nephritis to avoid early relapse.

Multicentric papillary renal carcinoma in renal allograft

A renal transplant recipient with 13 years of excellent allograft function was found incidentally to have a malignant mass in his transplanted kidney. After resection, pathological analysis showed 29 separate lesions of renal cell carcinoma. All tumors were confined within the renal capsule. The majority of tumors (21 of 29 tumors) were chromophil basophilic carcinoma with papillary architecture, 5 tumors were clear cell, 2 tumors were mixed cell type, and 1 tumor was chromophil eosinophilic papillary carcinoma. These histological findings are similar to those reported in hereditary papillary renal carcinoma. To our knowledge, this is the first case of multicentric papillary renal carcinoma occurring in the renal allograft. We speculate that the allograft in this case is predisposed to malignant changes because of preexisting genetic mutations, as well as prolonged immunosuppression.

Top 10 Things Primary Care Physicians Should Know About Maintenance Immunosuppression for Transplant Recipients

The success of organ transplantation allows many transplant recipients to return to life similar to nontransplant patients. Their need for regular health care, including preventive medicine, has switched the majority of responsibilities for their health care from transplant specialists to primary care physicians. To take care of transplant recipients, it is critical for primary care physicians to be familiar with immunosuppressive medications, their side effects, and common complications in transplant recipients. Ten subjects are reviewed here in order to assist primary care physicians in providing optimal care for transplant recipients.

Acute massive gentamicin intoxication in a patient with end-stage renal disease

A 65-year-old man with end-stage renal disease on continuous ambulatory peritoneal dialysis accidentally received an acute massive overdose of gentamicin as a treatment of peritonitis. The patient developed acute vestibular dysfunction and hearing loss following the overdose. His serum gentamicin had reached the extremely toxic level of 220 microg/mL. To remove the gentamicin, the patient received hemodialysis and hemoperfusion immediately. This was followed by two more courses of hemodialysis during the following 2 days. The gentamicin level was brought down to 10 microg/mL after the third hemodialysis. Moderate and persistent high-frequency hearing loss was documented with serial audiograms. The patient made a gradual but incomplete recovery from the vestibular dysfunction. The complications of gentamicin toxicity and its management are discussed with respect to our patient.

Brain Teaser: Encephalopathy After Stem Cell Transplantation

PRESENTATION In recent years, hematopoietic stem cell transplantation has been performed increasingly for a variety of hematologic disorders, solid tumors, and even nonmalignant disorders. One of our patients, a 53-year-old Hispanic woman with multiple myeloma, developed encephalopathy more than 1 week after autologous peripheral blood stem cell transplantation. She had received melphalan (200 mg/m) as the conditioning preparative regimen. On day 2 after the procedure, she had transient fever, and on day 6, she had mucositis. On day 8, she became confused and had a score of 8/15 on the Glasgow coma scale. She was intubated for airway protection on day 9.

Paradoxical Hypokalemia: Where Has All the Potassium Gone?

Paradoxical hypokalemia refers to a paradoxical drop in serum potassium level when potassium is given for severe hypokalemia. It was reported initially in a patient with thyrotoxic periodic paralysis. In this issue, Sung et al report paradoxical hypokalemia in patients with hypokalemic paralysis due to renal or gastrointestinal loss of potassium, or so called hypokalemic “nonperiodic” paralysis, a term used to distinguish it from hypokalemic periodic paralysis caused by an acute intracellular shift of potassium. Although hypokalemic nonperiodic paralysis has been well recognized, this is the first prospective study that provides the etiologies and responses to treatment of 58 cases, collected over 7 years at a tertiary medical center in Taiwan. The response to potassium replacement in hypokalemic nonperiodic paralysis and thyrotoxic periodic paralysis are markedly different (Table) due to different mechanisms of hypokalemia. The data on thyrotoxic periodic paralysis are taken from a similar prospective study by the same group of investigators. The presenting serum potassium levels and the potassium levels at time of recovery from paralysis are slightly lower in patients with nonperiodic paralysis, but these patients required fourfold greater potassium supplement and twice as much time to recover from paralysis. About 59% of thyrotoxic periodic paralysis patients developed rebound hyperkalemia, whereas no patients in the nonperiodic paralysis group did. Interestingly, 26% of thyrotoxic periodic paralysis and 55% of nonperiodic paralysis patients developed paradoxical hypokalemia after initial potassium infusion. Paradoxical hypokalemia is associated with higher systolic blood pressure, heart rate, and serum free T4 levels for the former; and higher serum renin activities and aldosterone levels for the latter. These findings suggest that paradoxical hypokalemia in thyrotoxic periodic paralysis is caused by more severe hyperthyroidism, whereas in nonperiodic paralysis, the culprit is volume depletion. The pathogenesis of hypokalemia and paralysis in patients with hypokalemic periodic paralysis has been elucidated due to the discovery of mutations in various ion

Phosphorus: another devil in our diet?

c t a a Serum phosphorus is probably the least ordered blood test among all electrolytes and minerals. Excessive phosphorus is toxic to the body by causing kidney and bone damage, vascular calcification, and premature ageing. Phosphorus toxicity is well documented in patients with end-stage renal disease. In this issue, Sim et al further reported the longerm outcomes associated with serum phosphorus levels in lmost 100,000 patients without significant chronic kidney