Abstract: Acute oxalate nephropathy (AON) is an increasingly recognized cause of acute kidney injury (AKI). Herein, we present two cases of biopsy-proven acute oxalate nephropathy in patients with gastrointestinal malabsorption, coincidentally both stemming from cholangiocarcinoma. The first is a 73-year-old male who presented with syncope and was found to have severe, oliguric AKI in the setting of newly diagnosed, nonresectable cholangiocarcinoma. The second is a 64-year-old man with remote resection of cholangiocarcinoma who presented after routine laboratory monitoring showed significant AKI. Temporary dialysis was required in both cases before renal recovery occurred. Together, these cases should increase physicians’ suspicion of AON in the presence of malabsorption. By doing so, the workup of oxalate nephropathy can be expedited with prompt initiation of treatment. PubDate: Sun, 23 Dec 2018 08:13:43 +000
Abstract: Peritonitis is a very serious complication encountered in patients undergoing peritoneal dialysis and healthcare providers involved in the management should be very vigilant. Gram-positive organisms are the frequent cause of peritonitis compared to gram-negative organisms. There has been recognition of peritonitis caused by uncommon organisms because of improved microbiological detection techniques. We report a case of peritonitis caused by Moraxella osloensis (M. osloensis), which is an unusual cause of infections in humans. A 68-year-old male, who has been on peritoneal dialysis for 2 years, presented with abdominal pain and cloudy effluent. Peritoneal fluid analysis was consistent with peritonitis and peritoneal fluid culture grew gram-negative bacteria. M. osloensis was identified by 16 S PCR phenotypic and sequencing techniques. Patient responded well to the treatment, with intraperitoneal cephalosporin, and repeat peritoneal fluid culture yielded no growth. M. osloensis rarely causes infection in humans and responds well to treatment, as reported in literature. PubDate: Thu, 20 Dec 2018 08:14:28 +000
Abstract: We report a pediatric patient with atypical hemolytic uremic syndrome due to a C3 gain-of-function mutation diagnosed in infancy. She was treated from the start with a constant dose of 300 mg eculizumab every second week from the onset and followed by routine complement analyses for six years. Her complement system was completely inhibited and the dose interval was prolonged from 2 to 3 weeks without alteration of the dose and the complement activity continued to be completely inhibited. Blood samples taken immediately before, immediately after, and between eculizumab doses were analyzed for eculizumab-C5 complexes and percentage of total complement activity, using the Wieslab® test, and compared to a pool of sera from 20 healthy controls. The patient exhibited complete complement inhibition at all three time-points and had no free circulating C5 suggesting there was complete binding to eculizumab. She has now been treated for six years with full complement blockade. We suggest therefore that analysis of complement activity using the Wieslab® test is useful for evaluating the effect of eculizumab when dose intervals are prolonged. PubDate: Tue, 18 Dec 2018 07:01:10 +000
Abstract: Background. Pulmonary-renal syndrome is characterised by acute kidney injury, haematuria, and haemoptysis and is a well-recognised presentation of diseases such as ANCA vasculitis that require urgent immunosuppression. Case Presentation. A patient presented with a brief history of haemoptysis, acute renal failure, microscopic haematuria, and severe hypertension. The diagnosis was initially not clear so he was treated with antihypertensives, renal replacement therapy, and immunosuppression. Renal biopsy subsequently showed evidence of malignant hypertension. Autoantibodies were uniformly negative. Conclusions. This case demonstrates that malignant hypertension can present as pulmonary-renal syndrome. PubDate: Mon, 17 Dec 2018 07:10:59 +000
Abstract: We describe a case of biopsy-proven dabigatran related nephropathy in a patient without underlying IgA nephropathy. To date, dabigatran related nephropathy was only reported in patients with concurrent or undiagnosed IgA nephropathy, suggesting that it may predispose patients to dabigatran associated injury. The patient is an 81-year-old woman with multiple medical comorbidities, including nonvalvular atrial fibrillation, who was anticoagulated with dabigatran. She presented to hospital with acute kidney injury in the setting of volume overload. Her estimated glomerular filtration rate decreased from a baseline of 57 mL/min/1.73 m2 to 4 mL/min/1.73 m2, necessitating hemodialysis. Renal ultrasound findings, fractional excretion of sodium, and urinalysis suggested acute kidney injury. Renal biopsy showed acute tubular injury, tubular red blood cell casts, and an absence of active glomerulonephritis, similar to the pathological findings of warfarin related nephropathy. A diagnosis of anticoagulant related nephropathy secondary to dabigatran was therefore established. This case demonstrates that dabigatran, like warfarin, may increase tubular bleeding risk in patients, irrespective of underlying kidney or glomerular disease. PubDate: Sun, 09 Dec 2018 08:01:08 +000
Abstract: Malignancy associated lactic acidosis is a rare metabolic complication that may accompany various types of malignancies. To date, most cases that have been reported are associated with hematologic malignancies (lymphoma and leukemia). Many theories have been proposed to explain the pathophysiology of lactic acidosis in malignancies. We are reporting an unusual case of a 62-year-old female who presented with a complaint of generalized weakness. Patient was found to have pancytopenia and metabolic acidosis with an anion gap secondary to lactic acid in addition to non-anion gap acidosis (NAGA). The lactic acidosis resolved only after initiation of chemotherapy as she was diagnosed with B-cell acute lymphoblastic leukemia. Our patient also had a coexistent Renal Tubular Acidosis (RTA) with large kidneys. The kidney size also decreased with chemotherapy. Our case is unique as evidenced by aleukemic leukemia combined with anion gap acidosis and non-anion gap acidosis. Lactic acidosis has many different causes; although rare, hematologic malignancies should be included in the differential diagnosis regardless of cell counts or tumor burden. PubDate: Sun, 18 Nov 2018 06:38:46 +000
Abstract: Metformin-associated lactic acidosis [MALA] is a potentially fatal condition characterized by an elevation in serum lactate in patients with metformin exposure. An 82-year-old man with no prior renal history was brought to hospital after being found by his family in a confused state. He had a history of type 2 diabetes mellitus, and his medications included regular metformin. On arrival to our hospital he was conscious but confused and noted recent decreased oral intake. Initial investigations revealed severe acidemia (pH PubDate: Thu, 15 Nov 2018 07:26:37 +000
Abstract: Background. Hypocalcaemia is increasingly recognized as a complication of denosumab use in Chronic Kidney Disease (CKD) patients with osteoporosis. Despite Therapeutic Goods Administration (TGA) notifications in 2013, we have subsequently encountered several cases of denosumab-induced hypocalcaemia, raising concern about lack of widespread awareness among prescribing practitioners. Aims. We reviewed the morbidity and healthcare intervention needs of CKD patients with hypocalcaemia attributed to denosumab. Methods. A retrospective case series of CKD patients with clinically significant hypocalcaemia after exposure to denosumab, encountered at the tertiary care referral hospital from December 2013 to February 2017, was undertaken. Results. Eight patients (52-85 years of age) with stage 4-5 CKD developed clinically significant hypocalcaemia (corrected calcium 1.45±0.21mmol/L) following denosumab therapy for osteoporosis. Seven of the eight patients required inpatient management with three patients requiring intravenous calcium replacement and cardiac monitoring in a high dependency unit. Our study also identified additional factors that could potentially contribute to hypocalcaemia such as lack of calcium supplementation, use of noncalcium based phosphate binders, absence of or use of lower doses of calcitriol supplementation, low vitamin D levels, concomitant treatment with loop diuretics, history of parathyroidectomy, or presence of acute medical illness. Conclusion. Multiple cases of severe hypocalcaemia in CKD patients following denosumab exposure were encountered after TGA warnings, resulting in considerable morbidity and intensive healthcare interventions in CKD patients. We advocate greater awareness amongst the medical profession, careful consideration before using denosumab in CKD patients, and close follow-up after administration to prevent morbidity. PubDate: Sun, 04 Nov 2018 09:13:12 +000
Abstract: Neonatal jaundice is considered one of the most common reasons for admission to the pediatric medical ward. We report a case of a 1-month-old infant who presented with jaundice but no fever or any other signs of systemic illnesses. Laboratory test results revealed high direct hyperbilirubinemia, and urine culture showed a urinary tract infection with Enterobacter cloacae as the causative agent. He was admitted to the pediatric medical ward where he was treated with a course of antibiotics for 14 days, and cholestasis resolved completely following a course of antibiotics. We conclude that direct hyperbilirubinemia can be related to urinary tract infection in neonates. It is unusual for urinary tract infection to present clinically and biochemically as cholestatic jaundice. PubDate: Wed, 24 Oct 2018 06:43:56 +000
Abstract: We had the challenged to treat a 40-year-old female with Systemic Scleroderma who was showing unspecific symptoms. During her time at the hospital she rapidly develops renal dysfunction, associated with hypertension. She required renal replacement therapy initiation and we observed a decline in hemoglobin and platelets numbers. We confirm a microangiopathic hemolytic anemia and rule out other immune diseases or thrombotic thrombocytopenic purpura. Systemic Sclerosis is a chronic immune disorder of unknown origin that it is not completely understood. It is believed that environmental factors may contribute and also altered genes may be implicated in the immune system’s function. Microangiopathic hemolytic anemia occurs in 43% of patients who develop scleroderma renal crisis and an activation of the complement system through the classical pathway may be involved. Given that context we decided to treat the patients with C5 blocker Eculizumab and obtain an extraordinary positive response. PubDate: Tue, 23 Oct 2018 06:20:53 +000
Abstract: Sjögren’s syndrome is an autoimmune disease with multisystem involvement and varying clinical presentation. We report the clinical course and outcome of a case who presented with repeated episodes of hypokalemia mimicking hypokalemic periodic paralysis and metabolic acidosis, which was later diagnosed as distal renal tubular acidosis secondary to primary Sjögren’s syndrome. A 50-year-old lady, who was previously diagnosed as hypokalemic periodic paralysis, presented with generalized weakness and fatigue. She was found to have severe hypokalemia with normal anion-gap metabolic acidosis consistent with distal renal tubular acidosis. Subsequent evaluation revealed Sjögren’s syndrome as the cause of her problems. Kidney biopsy done to evaluate significant proteinuria revealed nonproliferative morphology with patchy acute tubular injury and significant chronic interstitial nephritis. The patient responded well to potassium supplementation and oral prednisolone. Presentation of this case highlights the necessity of close vigilance while managing a case of repeated hypokalemia, which could be one of the rare clinical manifestations of Sjögren’s syndrome. PubDate: Tue, 16 Oct 2018 08:10:28 +000
Abstract: Turbid dialysate in a patient on peritoneal dialysis is usually due to peritonitis and almost all these patients are started on empirical antibiotics pending cultures. However, in few of them with culture negative fluid, this could represent other etiologies like chyle, which requires more intensive investigations, and analysis of fluid itself reveals some rare diagnosis. We present one such report of chylous ascites with prompt investigation leading to a diagnosis of malignancy in a peritoneal dialysis patient. PubDate: Tue, 09 Oct 2018 08:31:24 +000
Abstract: Glomerular immunoglobulin A (IgA) deposition is a common finding in hepatic glomerulosclerosis; thus, this disease is also called hepatic IgA nephropathy. However, only a small number of patients with hepatic IgA nephropathy have active glomerular lesions, so functional decline is slow in most cases. In this report, we describe a 60-year-old man who developed nephrotic syndrome and progressive renal impairment during follow-up for alcoholic liver cirrhosis. A renal biopsy showed a membranoproliferative glomerulonephritis-like pattern; diffuse double-contours of the glomerular basement membrane and focal active glomerular lesions with moderate-to-severe endocapillary proliferation and fibrocellular crescents. Immunofluorescence findings revealed granular staining for monoclonal IgA1-κ and C3 on the peripheral capillary walls. Laboratory examinations did not reveal any definitive evidence of myeloproliferative disorders. Therefore, this case may represent a previously unrecognized etiology of renal injury in relation to liver cirrhosis that is characterized by monoclonal IgA1-κ deposits and proliferative glomerulonephritis. PubDate: Mon, 01 Oct 2018 06:45:13 +000
Abstract: Hyponatremia is a well-known medication related side effect of selective serotonin reuptake inhibitors; despite its association with escitalopram, the newest SSRI is very rare. We did a review of literature and came across only 14 reported case of this rare association of SIADH with escitalopram. We hereby report a case of a 93-year-old female who presented with generalized tonic-clonic seizure and was diagnosed with severe hyponatremia due to escitalopram-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH). With this article, we want to emphasize clinicians about this rare side effect of escitalopram use and look for the risk factors leading to SIADH. PubDate: Wed, 05 Sep 2018 07:50:50 +000
Abstract: Bartonella henselae is a fastidious organism that causes cat scratch disease, commonly associated with fever and lymphadenopathy but, in rare instances, also results in culture-negative infectious endocarditis. We describe a patient who presented with flank pain, splenic infarct, and acute kidney injury with an active urinary sediment, initially suspicious for vasculitis, which was subsequently diagnosed as B. henselae endocarditis. Bartonella endocarditis may present with a crescentic glomerulonephritis (GN) and elevated PR3-ANCA antibody titers, mimicking ANCA-associated GN, with 54 cases reported in the literature. Unique to our case in this series is a positive PR3-ANCA antibody despite a negative IIF-ANCA. Thus, the presentation of Bartonella can mimic ANCA-associated GN, and renal biopsy showing immune complex deposition is critical for diagnosis and appropriate treatment. PubDate: Sun, 19 Aug 2018 08:34:31 +000
Abstract: Glomerular diseases are one of the most frequent causes of chronic kidney disease, focal and segmental glomerulosclerosis being one of the commonest glomerulopathies. However, the etiology of this glomerular entity, which merely depicts a morphologic pattern of disease, is often not established and, in most of the patients, remains unknown. Nephrologists tend to assume focal and segmental glomerulosclerosis as a definitive diagnosis. However, despite the increasing knowledge developed in the field, genetic causes of glomerular diseases are currently identified in fewer than 10% of chronic kidney disease subjects. Moreover, unexplained familial clustering among dialysis patients suggests that genetic causes may be underrecognized. Secondary focal and segmental glomerulosclerosis due to genetic mutations mainly located in the podocyte and slit diaphragm can occur from childbirth to adulthood with different clinical presentations, ranging from mild proteinuria and normal renal function to nephrotic syndrome and renal failure. However, this histopathological pattern can also be due to primary defects outside the glomerulus. The present report illustrates an adult case of secondary focal and segmental glomerulosclerosis with a dominant tubulointerstitial damage that led to the pursue of its cause at the tubular level. In this patient with an undiagnosed family history of adult kidney disease, a genetic study unraveled a mutation in the mucin-1 gene and a final diagnosis of adult dominant tubular kidney disease-MUC1 was made. PubDate: Tue, 31 Jul 2018 06:44:31 +000
Abstract: Peritonitis is considered to be the most common complication of peritoneal dialysis (PD). It is usually caused by Gram positive Staphylococcus epidermidis. Achromobacter xylosoxidans (A. xylosoxidans) and Streptococcus suis (S. suis) are rare pathogens, but there is emerging evidence that they may be also responsible for PD related peritonitis. We described 2 cases of rare peritonitis treated in our center. In our opinion this is the first described case of PD related peritonitis caused by Streptococcus suis. PubDate: Mon, 30 Jul 2018 00:00:00 +000
Abstract: Antiphospholipid antibody syndrome (APS) may occur in a primary form or in association with SLE and seldom presents with nephrotic syndrome (NS). We present a case with APS who developed recurrent NS 6 years apart. The first episode of NS occurred with biopsy findings consistent with lupus nephritis (LN) class V (membranous) with no clear evidence of SLE, and responded to a remission with steroids and MMF. On the episode, the biopsy revealed negative immunofluorescent (IF) study for immune complexes and EM findings of complete effacement of foot processes and acellular debris in thickened capillary walls, compatible with healed previous episode of membranous LN and minimal change disease (MCD), a nonimmune complex podocytopathy. The episode responded to a partial remission, primarily with a short-term steroid therapy, and subsequently developed serologic evidence of SLE. Now there is growing evidence that a subset of SLE patients with NS are found to have MCD, likely due to podocyte injury caused by nonimmune complex pathway, called lupus podocytopathy. In LN, serial kidney biopsies often show transformation from one to another class of immune complex-induced glomerular lesions; however there are rare reports describing transformation of an immune complex to a nonimmune complex LN. Since the pathogenic mechanism of lupus podocytopathy is not delineated, and so far there are no reports on transformation of membranous LN, an immune complex nephropathy, to a nonimmune complex lupus podocytopathy, it still remains as a question whether our case with APS overlapping SLE had a concomitant membranous LN and lupus podocytopathy, or consequential membranous LN and lupus podocytopathy 6 years apart. PubDate: Tue, 24 Jul 2018 00:00:00 +000
Abstract: Two-stage revision total knee arthroplasty (TKA) is the standard of care for prosthetic joint infections. The first stage involves removal of the infected prosthesis and placement of an antibiotic impregnated cement spacer; following a period ranging from 4 weeks to 6 months, the spacer is then removed and replaced with a permanent prosthesis. The advantage to this approach is that antibiotic impregnated spacers provide supratherapeutic levels in the joint without toxic accumulation in serum. However, it remains important for physicians and pharmacists to be aware of antibiotic associated complications in knee revisions. We present a case of a two-stage revision total knee arthroplasty in which a cement antibiotic spacer caused acute renal failure and ultimately resulted in persistent chronic kidney disease without hemodialysis at 2 months’ follow-up. Our case reports the third highest serum tobramycin (13.7 mcg/ml) and second highest serum creatinine (8.62 mg/dl) for patients experiencing ARF due to an antibiotic spacer in two-stage revision TKA. PubDate: Mon, 02 Jul 2018 00:00:00 +000
Abstract: Difluoroethane is the active ingredient in various computer cleaners and is increasingly abused by teenagers due to its ease of access, quick onset of euphoric effects, and lack of detectability on current urine drug screens. The substance has detrimental effects on various organ systems; however, its effects on the kidneys remain largely unreported. The following case report adds new information to the developing topic of acute kidney injury in patients abusing difluoroethane inhalants. In addition, it is one of the first to show a possible relationship between prolonged difluoroethane abuse and the development of chronic kidney disease in the absence of other predisposing risk factors. PubDate: Thu, 07 Jun 2018 07:06:30 +000
Abstract: This is a case of a renal transplant recipient who developed a primary hepatic Burkitt lymphoma a few years after kidney transplantation. The past medical history of the patient was significant for anti-HCV positivity with liver histopathology showing minimal changes of grades 0 and 1, stage 0. She received a graft from a deceased donor, with rabbit antithymocyte globulin and methyl-prednisolone, as induction therapy, and was maintained on azathioprine, cyclosporine, and low dose methyl-prednisolone with normal renal function. Four years after KTx she presented with fatigue, hepatomegaly, and impaired liver function and the workup revealed multiple, variable-sized, low density nodules in the liver, due to diffuse monotonous infiltration of highly malignant non-Hodgkin lymphoma of B-cells, which turned out to be a Burkitt lymphoma. Bone marrow biopsy and spinal fluid exam were free of lymphoma cells. At time of lymphoma diagnosis she was shown to be positive for Epstein-Barr virus polymerase chain reaction. She received aggressive chemotherapy but died due to sepsis, as a result of toxicity of therapy. PubDate: Sun, 13 May 2018 08:52:01 +000
Abstract: Bacterial peritonitis is a common complication of peritoneal dialysis, but fungal peritonitis is unusual and is mostly due to Candida species. Peritonitis due to Histoplasma capsulatum is rare and we report one such case. A 63-year-old female presented with progressively worsening abdominal pain, fever, and altered mental status. She had end-stage renal disease and had been on peritoneal dialysis for 4 years. She had abdominal tenderness without rebound or guarding. Laboratory studies and CT of abdomen were significant for leukocytosis and peritoneal membrane thickening, respectively. Peritoneal dialysis fluid study was consistent with peritonitis and culture of the fluid grew Histoplasma capsulatum. Treatment recommendations include removal of catheter and initiation of antifungal therapy. With the availability of newer antifungals, medical management without removal of PD catheter is possible, but at the same time if there is no response to treatment within a week, PD catheter should be removed promptly. PubDate: Thu, 10 May 2018 00:00:00 +000
Abstract: Clostridium difficile infection is a rare precipitant of atypical haemolytic uraemic syndrome (aHUS). A 46-year-old man presented with watery diarrhoea following an ileocaecal resection. He developed an acute kidney injury with anaemia, thrombocytopaenia, raised lactate dehydrogenase, low haptoglobin, and red cell fragments. Stool sample was positive for C. difficile toxin B. He became dialysis-dependent as his renal function continued to worsen despite treatment with empiric antibiotics and plasma exchange. The ADAMTS13 level was normal consistent with a diagnosis of aHUS. The commencement of eculizumab led to the resolution of haemolysis and stabilisation of haemoglobin and platelets with an improvement in renal function. PubDate: Thu, 10 May 2018 00:00:00 +000
Abstract: Renal artery thromboembolism (RATE) is an uncommon complication of renal arteries from heart chamber. Although there is no treatment protocol prescribed with guidelines, thrombolytic agents such as rt-PA are frequently used. Unfortunately, current thrombolytic agent application protocol in treatment for the RATE is used in acute myocardial infarction or acute pulmonary embolism. In this protocol, 0.9–1.0% cerebral and 4–13% noncerebral hemorrhages are seen. In contrast to this protocol, we aimed to present a case of RATE, in which we applied low-dose, slow-infusion thrombolytic therapy, and we have not observed any complication such as cerebral and noncerebral hemorrhage. PubDate: Wed, 02 May 2018 08:07:11 +000
Abstract: Introduction. Sticky platelet syndrome (SPS) is a prothrombotic disease that is not well recognized and difficult to diagnose. Case Report. We present a case of a 49-year-old diabetic woman on ambulatory peritoneal dialysis therapy who underwent a kidney transplant from living-related donor. The donor was her sister with whom she shared one haplotype and absence of donor specific antibodies. The posttransplant evolution was torpid, developing progressive deterioration, which made us suspect a failure in the graft. Doppler ultrasound reported renal vein thrombosis and hypoperfusion of the renal artery. Without clinical improvement, she required a reintervention that ended in graftectomy, in which the histopathological report showed negative C4d with medullary and cortical infarction. Hematological studies were negative for antibodies against phospholipids, with correct levels of proteins C and S and antithrombin. Platelet aggregometry studies were carried out, which were compatible with SPS. Conclusions. Recognition of SPS in pretransplant studies is difficult if there is no history of previous thrombotic events. However, we must consider this entity in cases of acute thrombosis and loss of the graft of uncertain origin. PubDate: Sun, 22 Apr 2018 00:00:00 +000
Abstract: A 26-year-old African American male with a history of congenital cerebral palsy, sickle cell trait, and intellectual disability presented with abdominal pain that started four hours prior to the hospital visit. The patient denied fever, chills, diarrhea, or any localized trauma. The patient was at a party at his community center last evening and danced for 2 hours, physically exerting himself more than usual. Labs revealed blood urea nitrogen (BUN) level of 41 mg/dL and creatinine (Cr) of 2.8 mg/dL which later increased to 4.2 mg/dL while still in the emergency room. Urinalysis revealed hematuria with RBC > 50 on high power field. Imaging of the abdomen revealed no acute findings for abdominal pain. With fractional excretion of sodium (FeNa) > 3%, findings suggested nonoliguric acute tubular necrosis. Over the next couple of days, symptoms of dyspepsia resolved; however, BUN/Cr continued to rise to a maximum of 122/14 mg/dL. With these findings, along with stable electrolytes, urine output matching the intake, and prior use of proton pump inhibitors, medical decision was altered for the possibility of acute interstitial nephritis. Steroids were subsequently started and biopsy was taken. Biopsy revealed heavy deposits of myoglobin. Creatinine phosphokinase (CPK) levels drawn ten days later after the admission were found to be elevated at 334 U/dl, presuming the levels would have been much higher during admission. This favored a diagnosis of acute kidney injury (AKI) secondary to exertional rhabdomyolysis. We here describe a case of nontraumatic exertional rhabdomyolysis in a sickle cell trait (SCT) individual that was missed due to findings of microscopic hematuria masking underlying myoglobinuria and fractional excretion of sodium > 3%. As opposed to other causes of ATN, rhabdomyolysis often causes FeNa < 1%. The elevated fractional excretion of sodium in this patient was possibly due to the underlying inability of SCT positive individuals to reabsorb sodium/water and concentrate their urine. Additionally, because of their inability to concentrate urine, SCT positive individuals are prone to intravascular depletion leading to renal failure as seen in this patient. Disease was managed with continuing hydration and tapering steroids. Kidney function improved and the patient was discharged with a creatinine of 3 mg/dL. A month later, renal indices were completely normal with persistence of microscopic hematuria from SCT. PubDate: Sun, 15 Apr 2018 00:00:00 +000
Abstract: High flow arteriovenous fistulas are a common clinical entity affecting patients with end-stage renal failure receiving hemodialysis. Given the difficulty in predicting who will develop a high flow arteriovenous fistula the exact prevalence is unclear. We present two cases of patients with high flow arteriovenous fistula that developed clinical cardiac failure at a time point after the fistula was placed with findings of significant cephalic arch stenosis. Both patients required treatment of cephalic arch stenosis with balloon angioplasty with subsequent surgical aneurism resection. Accurate and timely diagnosis of high flow arteriovenous hemodynamics by prospective monitoring of volumetric flow and cardiac function is required to halt this process prior to cardiac compromise. PubDate: Tue, 10 Apr 2018 00:00:00 +000
Abstract: Rifampicin is a key component of multidrug regimens not only for tuberculosis, but also nontuberculous mycobacterial infections (NTM) which are on the rise worldwide. Knowledge of the toxicity profile is important. Hepatotoxicity is a well-known side effect of Rifampicin necessitating regular liver function monitoring during therapy. Acute kidney injury (AKI) is a relatively rare complication, usually resulting from allergic interstitial nephritis (AIN). Rifampicin-induced intravascular hemolysis resulting in hemoglobinuria and AKI is even more uncommon, especially in Western countries with low prevalence of mycobacterial infections. Rifampicin-induced antibodies are implicated and this complication preferentially occurs during intermittent drug treatment protocols or when Rifampicin is restarted after a long drug-free interval. Awareness of this drug complication and its unique timing is important especially among emergency room physicians where patients with AKI may first present. It is equally important for nephrologists and pathologists. We describe one such case with detailed clinical course of the patient and interesting biopsy findings of ATN with intratubular hemoglobin casts. PubDate: Thu, 05 Apr 2018 00:00:00 +000
Abstract: De novo thrombotic microangiopathy (TMA) can occur after kidney transplantation. An abnormality of the alternative pathway of complement must be suspected and searched for, even in presence of a secondary cause. We report the case of a 23-year-old female patient who was transplanted with a kidney from her mother for end-stage renal disease secondary to Hinman syndrome. Early after transplantation, she presented with 2 episodes of severe pyelonephritis, associated with acute kidney dysfunction and biological and histological features of TMA. Investigations of the alternative pathway of the complement system revealed atypical haemolytic uremic syndrome secondary to complement factor I mutation, associated with mutations in CD46 and complement factor H related protein genes. Plasma exchanges followed by eculizumab injections allowed improvement of kidney function without, however, normalization of creatinine. PubDate: Wed, 14 Mar 2018 00:00:00 +000
Abstract: End stage renal disease (ESRD) population account for 1.9 per patient year of hospital admissions annually. ESRD population are at increased risk of bleeding secondary to use of anticoagulation during hemodialysis and uremia induced platelet dysfunction. Gastrointestinal bleeding accounts for 3–7% of all deaths in ESRD population. Lower gastrointestinal bleeding refers to blood loss from a site in the gastrointestinal tract distal to the ligament of Treitz. It is usually suspected when a patient complains of hematochezia. It is different from patients presenting with hematemesis that suggests bleeding from upper gastrointestinal tract. Common causes of lower gastrointestinal bleed include diverticulosis, ischemia, hemorrhoids, neoplasia, angiodysplasia, and inflammatory bowel disease. ESRD patients are known to retain phosphate alone or in combination with calcium which has been associated with high mortality. Sevelamer is a phosphate binder used widely in ESRD population. The known side effects of sevelamer include metabolic acidosis, vomiting, nausea, diarrhea, dyspepsia, abdominal pain, constipation, flatulence, fecal impaction, and skin rash. We are reporting a unique case of a 56-year-old female with end stage renal disease on sevelamer hydrochloride who presented with gastrointestinal bleeding and underwent a right hemicolectomy found to have sevelamer-induced mucosal ulceration and crystal deposition in the colonic mucosa. This case report highlights the fact that, with widespread use of this medication in the patients with chronic kidney diseases, physicians should be aware of this underrecognized entity in the differential diagnosis of gastrointestinal bleed in ESRD patients. PubDate: Wed, 28 Feb 2018 11:08:23 +000
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