Clinical Nephrology. Case Studies最新文献

We recently encountered concern about the safety of bariatric surgery for a patient with cystinuria. Bariatric surgery procedures include those that cause malabsorption, like the Roux-en-Y gastric bypass procedure, and restrictive operations, such as the sleeve gastrectomy. These procedures produce beneficial effects on health and life expectancy, though whether kidney stones are prevented, as well as promoted, is not established. Although the importance of body weight to metabolic stone activity in patients with cystinuria is not established, the patient's physicians were concerned about whether any bariatric surgery procedure would affect her ability to drink sufficient quantities of water in order to reduce stone activity. Here we report the experience of a genetically defined patient with cystinuria who underwent a gastric sleeve procedure. In the months after the procedure, she lost 45 kg, though with time she regained 23 kg of that loss. She was able to maintain a urine volume of 4.0 L per day and has had no stone recurrence.

Introduction: Lactic acidosis (LA) can be categorized as type A, which occurs in the presence of tissue hypoxia, or type B, occurring in the absence of tissue hypoxia. Hematologic malignancies are an uncommon cause of type B LA.

Case presentation: A 63-year-old man, HIV-negative, with a history of diabetes mellitus, hypothyroidism, and non-alcoholic fatty liver disease (NAFLD), presented to the ED complaining of acute-on-chronic lumbar pain, and was found to have high serum anion gap (AG) LA. The rest of chemistry and infectious workup was within normal limits. Despite bicarbonate therapy and fluid resuscitation, the patient remained with persistent AG metabolic acidosis and increasing lactic acid up to 14.5 mmol/L. An abdominal computerized tomography (CT) revealed multiple bilateral enhancing lesions in the kidneys, as well as gastric wall thickening. Upper gastrointestinal endoscopy with biopsy showed a high-grade Burkitt's lymphoma. Further staging showed bone marrow involvement and extensive abdominal adenopathy. After two cycles of inpatient chemotherapy with dose-adjusted EPOCH-R (etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin and rituximab), the patient developed multifocal pneumonia complicated by respiratory failure. Following a prolonged ICU stay, after discussion with the family members, a decision of withdrawal of life-sustaining therapy was reached.

Conclusion: Persistent LA, without identifiable causes of tissue hypoxia, should prompt clinicians to suspect non-hypoxic etiologies, including occult high-grade malignancies. Hematological malignancies constitute an extremely rare cause of type-B LA, carrying a poor prognosis.

A 3-year-old girl came to our attention for fever and upper respiratory tract infection associated with thrombocytopenia, non-immune hemolytic anemia, and acute kidney injury (AKI). Complete blood count and renal function slowly normalized, with no need for dialysis. She was always normotensive with valid diuresis; her neurological status also rapidly improved. Nasal swab turned out positive for influenza A H1N1; stool test was negative for Shiga toxin-producing Escherichia coli (STEC). The patient was treated with oseltamivir for 5 days with a favorable outcome. Association between hemolytic uremic syndrome (HUS) and H1N1 influenza is poorly reported in literature [1, 2, 3, 4]. The pathogenic role of the virus in causing HUS is still controversial and debated [1, 2, 3, 4]. In our patient, complement activity markers (serum C3 and C5b-9) alteration suggested a transient, virus-mediated complement activation.

Burkitt's lymphoma is a common cause of tumor lysis syndrome (TLS) and, in the era of aggressive utilization of prophylactic allopurinol and recombinant uricase enzyme, nephrologists are increasingly witnessing monovalent or divalent cation abnormalities without marked uric acid elevation. An 18-year-old male received his 1^st cycle of intensive chemotherapy for Burkitt's lymphoma and developed TLS as defined by the Cairo Bishop criteria. Lactate dehydrogenase peaked at 9,105 U/L (range: 130 - 250) and was accompanied by acute kidney injury, including serum creatinine 2.2 mg/dL on the 4^th day with oliguria, hyperkalemia, extreme hyperphosphatemia (21.4 mg/dL), hypermagnesemia, and hypocalcemia. Renal replacement therapy decision was made based on life-threatening electrolyte disturbances. The competing necessity to effectively control hyperphosphatemia and avoid the complication of dialysis disequilibrium syndrome prompted us to perform an initial intermittent hemodialysis with simultaneous intravenous mannitol administration, followed by continuous hemodialysis to manage the continued production of phosphorus from cell lysis. Osmotic stability during the therapy session was affirmatively demonstrated (322, 319 mOsm/kg, respectively). The patient showed excellent tolerance for these therapies and eventually recovered renal function as demonstrated during follow-up visits.

Background: Increased incidence of kidney injury has been seen in patients with COVID-19. However, less is known about COVID-19 susceptibility and outcomes in end-stage renal disease (ESRD) patients on hemodialysis (HD). Reduced angiotensin-converting enzyme 2 (ACE-2) from SARS-CoV-2 binding and increased angiotensin II (Ang-II) activity have been suggested as mechanisms for COVID-19 renal pathophysiology.

Materials and methods: In this case series, we analyzed the data of 3 patients with ESRD who had a delay in receiving their regular HD. Reduced oxygen requirement, resolved hyperkalemia, and normalized fluid status were used for the basis of discharge.

Results: Presenting symptoms included fever, dyspnea, and dry cough. Laboratory markers were characteristic for COVID-19, such as lymphopenia, elevated D-dimer, C-reactive protein (CRP), and interleukin 6 (IL-6). All 3 of our reported patients required urgent HD upon admission. However, we report no fatalities in our case series, and our patients did not have a severe course of illness requiring endotracheal intubation. We reviewed COVID-19 pathophysiology and how patients with ESRD on HD may be particularly at risk for infection.

Conclusion: New renal failure or ESRD sequelae, such as hyperkalemia, uremic encephalopathy, and fluid overload, can be exacerbated by a delay in receiving HD due to COVID-19 infection. Both direct COVID-19 infection and the challenges this pandemic creates to health care logistics present unique threats to ESRD patients on HD.

Introduction: Cutaneous manifestations related to chronic kidney disease (CKD) are common and associated with high morbidity. Acquired perforating dermatosis (APD) occurs mostly in diabetic or CKD patients, namely those undergoing hemodialysis.

Case report: A 58-year-old male with type 2 diabetes, with long-term insulin use, several microvascular and macrovascular complications, and on maintenance hemodialysis for 5 years presented with a 1-week history of painful, pruritic, umbilicated papules and some punctiform necrotic lesions on his left forearm, both hands, and both amputation stumps. There was no evidence of infection or vascular alterations, and the patient was not responsive to an initial course of topical corticosteroid. These lesions rapidly evolved to larger, coalescent necrotic injuries, with aggravated pain, intense left-hand skin peeling, and the appearance of similar lesions in the trunk, requiring hospital admission. Calciphylaxis and APD were suspected. Skin biopsy was performed and directed treatment initiated, including intradialytic sodium thiosulfate. Histology findings were compatible with APD and also excluded findings suggestive of vasculitis or calciphylaxis. Soon after, difficult-to-treat cellulitis of the left hand and forearm progressed to critical ischemia and amputation. Microbiology analysis revealed Serratia marcescens as the causative agent.

Discussion: To our knowledge, there are no previously described cases of APD-related cellulitis. Its treatment can be particularly challenging, as lesions can persist and relapse, and chronic scars can develop. S. marcescens behaves as an opportunistic and difficult-to-treat pathogen, complicating the prognosis.

Conclusion: APD can be associated with cellulitis and all of its complications in patients with underlying severe vasculopathy. Awareness of this complication in APD with early referral and aggressive treatment might improve the outcomes and quality of life of such patients.

Background: Allograft renal vein thrombosis can cause graft loss during the early postoperative period. This diagnosis is sometimes elusive, requiring a strong suspicion. On the other hand, several authors have recognized risk factors for allograft renal vein thrombosis, but neither a preventive approach nor a treatment have been recommended for this complication.

Case presentation: We present a case report of early allograft renal vein thrombosis, preceded by femoral common deep vein thrombosis in a recipient of a third kidney transplant. Despite femoral common deep vein thrombosis treatment with low-molecular-weight heparin and progressive improvement of renal function to a nadir serum creatinine of 0.51 mg/dL, the patient experienced a sudden episode of anuria on postoperative day 5. Doppler ultrasonography strongly suggested the diagnosis of allograft renal vein thrombosis. The patient underwent balloon catheter and aspiration venous thrombectomy, followed by unfractionated heparin perfusion. After 4 days of anuria and multiple blood transfusions, when allograft nephrectomy was contemplated, diuresis suddenly resumed. After 1 year of follow-up, the patient still has a normal renal function.

Conclusion: This case report shows successful treatment of allograft renal vein thrombosis associated with deep vein thrombosis in the first week of transplantation, using balloon catheter and aspiration venous thrombectomy followed by perfusion of unfractionated heparin. The authors suggest this technique as a treatment option for transplant renal vein thrombosis. However, they reinforce the importance of individualized treatment and they remind that a delay may jeopardize the potential benefit of the procedure.

Cerebral salt wasting (CSW) is an uncommon cause of hyponatremia characterized by extracellular volume depletion, high urine sodium concentration and osmolality, and low serum uric acid concentration in association with central nervous system (CNS) disease. Distinguishing CSW from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a much more common form of hyponatremia in this setting, can be challenging because both present with identical laboratory features. However, treatment of CSW and SIADH differs, making a correct diagnosis important. Here we present a case of CSW in a 75-year-old man in whom severe hyponatremia and volume depletion were discovered in the setting of traumatic head injury and Dandy-Walker malformation of the brain, a rare congenital brain malformation. Treatment with intravenous normal saline and later oral salt supplementation and fludrocortisone was successful.

Introduction: Though respiratory, immune, and coagulation systems are major targets of coronavirus disease 2019 (COVID-19), kidney dysfunction, presenting with acute kidney injury (AKI), is also common. Most AKI cases in COVID-19 manifest as acute tubular injury (ATI) in conjunction with multiorgan failure. While initial renal pathological findings were limited to acute tubular necrosis and collapsing glomerulopathy, a recent case series reported a larger spectrum of findings.

Case report: Here, we report a case of membranous nephropathy (MN) in an 81-year-old Hispanic man with underlying chronic kidney disease (CKD) stage 3 who developed ATI in the setting of COVID-19. The patient was hospitalized for hypoxic respiratory failure in the setting of AKI stage 3 with serum creatinine 7.1 mg/dL 6 days after a positive-SARS-CoV-2 screening. He was found to have nephrotic range proteinuria, glycosuria (with normal serum glucose), anemia, and hypoalbuminemia. Kidney biopsy showed ATI and early MN. Workup for primary and secondary MN was unrevealing, and serum PLA2R antibody was negative. No viral particles were observed in podocytes.

Conclusion: Although the MN could be incidental, this observation raises the question of whether SARS-CoV-2 infection can trigger or worsen an underlying MN from an exaggerated immune response associated with COVID-19.

Hypercalcemia is a frequently encountered electrolyte abnormality with a well-described differential diagnosis and classic algorithm for evaluation. The treatment for hypercalcemia is dependent on the underlying etiology. Hypervitaminosis D is an uncommon cause of hypercalcemia, but the use of vitamin D supplementation has expanded and case reports of supplemental vitamin D induced hypercalcemia have become more frequent. We present a case of hypervitaminosis D-induced altered mental status where diagnosis was delayed and additional invasive testing was performed due to an assumption regarding phosphatemia.