Case Reports

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NEPHROLOGY 2014; 19 (Supp. 4), 89–97

doi:10.1111/nep.12303

CASE REPORTS 273 DAPTOMYCIN IS EFFECTIVE FOR INTRACTABLE VASCULAR GRAFT INFECTION BY METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS: A CASE REPORT H DEGUCHI, Y MORI, KOKI TOKUNAGA, S TAKENOUCHI, Y MISHIGE, A NAKASHIMA Imamura byoin-bunin, Kagoshima, Japan Background: Graft infection is sometimes critical for patients receiving hemodialysis therapy. Especially, Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most trouble species. We present a case of graft infection of MRSA and successful treatment with Daptomycin. Case Report: A 77-year-old female, who had been receiving hemodialysis therapy 3 times a week due to end stage renal failure, was admitted to our hospital complaining of fever and shaking chill. Synthetic vascular prosthesis (expanded polytetrafluoroethylene) was used for vascular access. Her skin on graft turned red and swollen with exudate and a little pus. Urine analysis showed bacteria by Gram staining. We diagnosed these phenomena as vascular graft infection and urinary tract infection. We administered antibiotics, Ceftriaxone for urinary tract infection and Vancomycin for graft infection. Bacteria disappeared on urine analysis and we discontinued using Ceftriaxone. MRSA was found by blood culture, and we continued using Vancomycin. Transthoracic echocardiography revealed no apparent vegetation. As we continued administering Vancomycin, swollen and reddened skin turned normal, but MRSA was positive on blood culture. We changed antibiotics, Vancomycin to Daptomycin. By changing antibiotics, blood culture turned negative. After administered antibiotics for 4 weeks, she was discharged and moved to another hospital to receive rehabilitation. Conclusions: Sometimes MRSA forms a biofilm. Vancomycin doesn’t permeate a biofilm through inside easily. Daptomycin, however, penetrate through inside and show antibacterial activity. In our case, successful treatment was done with Daptomycin. Daptomycin is one of the choice to treat graft infection by MRSA when it is intractable.

274 A CASE REPORT OF 2 SUCCESSFUL PREGNANCY OUTCOMES IN A FEMALE WITH END STAGE RENAL FAILURE SECONDARY TO FOCAL SEGMENTAL GLOMERULOSCLEROSIS S AGGARWAL1, S ROXBURGH1, A MATHER1, S MCGINN1, S SEEHO2, T NIPPITA2, M BROWN3 1 Renal Medicine, Royal North Shore Hospital, St Leonards, NSW; 2Obstetrics and Gynaecology, Royal North Shore Hospital, St Leonards, NSW; 3Renal Medicine, St George Hospital, Kograh, NSW, Australia Background: Successful pregnancy outcomes have been increasingly reported in patients with end stage kidney disease (ESKD) with improved haemodialysis regimes. We report 2 successful pregnancies in a 32 year old female with ESKD on chronic haemodialysis. Case Report: Our patient developed ESKD secondary to focal segmental glomerulosclerosis (FSGS) that was treated unsuccessfully with cyclophosphamide and steroids and progressed to dialysis by age 20. She subsequently had a renal transplant aged 25 with disease recurrence resulting in a return to nocturnal haemodialysis within 12 months. In 2009 she conceived and was managed with extended dialysis hours (36 hours/week with an average urea of 6 mmol/L) and correction of anaemia with increased dose of erythropoietin stimulating agents. At 33 + 6/40 gestation she developed preterm premature rupture of membranes (PPROM). She delivered a 2.3 kg male who developed severe nephrotic syndrome which resolved spontaneously by day 30. Genetic testing of both the mother and child did not reveal a familial or genetic form of FSGS. In 2012 she successfully progressed with a pregnancy after 2 miscarriages at 8/40 gestation. She remained on haemodialysis for 36 hours/week with an average urea of 4–6 mmol/L and a haemaglobin greater than 95 g/L. At 28 + 4/40 gestation she developed PPROM and went into spontaneous labour at 34 + 3/40 gestation. She delivered a 1.7 kg male with no evidence of nephrotic syndrome. Conclusions: This case supports the literature showing that extended hours of haemodialysis and correction of anaemia can preserve fertility and allow successful pregnancy outcomes in women on haemodialysis. The development and resolution of neonatal nephrotic syndrome in the first infant supports the hypothesis that injury to the glomerular cells in FSGS may be due to a circulating permeability factor.

275 RENAL (AND HERPETIC) RE-TRANSPLANTATION S SETYAPRANATA1, KJ WIGGINS1, SG HOLT1,2, WR MULLEY3, PG KERR3, AJ LANDGREN1, A YOUNG4, H OPDAM4, A ROBERTSON1, PD HUGHES1 1 Royal Melbourne Hospital, Melbourne, Victoria; 2The University of Melbourne, Melbourne, Victoria; 3Monash Medical Centre, Melbourne, Victoria; 4Donate Life Victoria, Melbourne, Victoria, Australia Aim: Case report of renal re-transplantation, reported only once previously. Report: A middle aged recipient received a kidney transplant from a deceased multi-organ donor. After initially doing well, the patient suffered cardiac arrest several days post-operatively and sustained hypoxic brain injury and was declared brain dead. Following the family’s consent, the allograft kidney was retrieved and re-transplanted into a man with end-stage renal failure secondary to reflux nephropathy. The lungs were used in a separate recipient but the liver was not transplanted due to suspicion of fatty changes based on macroscopic appearance. Histological analysis of the liver more than 24 hours after transplantation of the other organs revealed coagulative parenchymal necrosis with nuclear inclusions and moderate parenchymal cholestasis, suggestive of herpes viral hepatitis. Examination of the renal implantation biopsy showed histiocytes with enlarged nuclei containing viral inclusions in the capsular fibrous tissue, with positive immunostaining for herpes simplex virus (HSV). Valaciclovir was started immediately after obtaining histological evidence of donor HSV infection and this was subsequently converted to intravenous ganciclovir. Our recipient had pre-formed IgG antibodies to HSV-1 and HSV-2, and was IgM negative pretransplant. HSV viraemia was detected day 5 post-transplant with a viral load of 7688 copies/mL by polymerase chain reaction (PCR) assay. He completed a 30-day course of intravenous ganciclovir before switching to valganciclovir as standard cytomegalovirus prophylaxis. The HSV PCR became undetectable on day 7 of IV ganciclovir and has remained undetectable. The patient remains well with an estimated glomerular filtration rate of 61 mL/min/1.73 m2 and further investigation of the apparent viral transmission is underway. Conclusions: We report good short term results of renal re-transplantation and HSV transmission by transplantation.

276 ACUTE KIDNEY INJURY DUE TO DECOMPRESSION ILLNESS A VIECELLI, J JAMBOTI, P FERRARI Department of Nephrology, Fremantle Hospital, Perth, Western Australia, Australia Background: Decompression illness is a rare but serious complication of diving caused by intravascular or extravascular gas bubble formation. Case Report: We report the first case of acute kidney injury in a 27-year-old diver caused by arterial gas emboli formation following three rapid uncontrolled ascents. He presented with transient neurological symptoms including confusion and paralysis followed by abdominal pain (initial lactate 10.8 mmol/L) and rapidly evolving acute kidney injury due to acute tubular necrosis (ATN; initial creatinine 120umol/L, peak at 1210umol/L on day 4 post-diving accident). The diagnosis of ischaemia-induced ATN was supported by a high urinary fractional sodium excretion of 5.5%, elevated LDH (486U/L [125–250]) and a MAG3 scan in keeping with ATN. The absence of myoglobinuria and only moderately elevated creatine kinase (maximum 893U/L [30–170]) made rhabodmyoloysisinduced ATN unlikely. He received supportive care with intravenous hydration, sodium bicarbonate and 100% oxygen followed by 7 sessions of hyperbaric therapy and recovered fully without needing dialysis. Conclusions: Arterial air embolism occurs when expanding gas ruptures alveolar capillaries (pulmonary barotrauma) and enters the arterial circulation as a result of rapid decompression. Clinical manifestations depend on the site of embolization and usually include neurological and respiratory symptoms but can also involve the muscles, skin, mesenteric circulation and as shown in this case the kidneys. The diagnosis is made on clinical grounds since gas bubbles are rarely detectable on imaging. Best first aid for decompression illness is 100% oxygen therapy and supportive care but early transfer to a hyperbaric treatment unit is important as symptoms may evolve over time as in our patient.

© 2014 The Authors Nephrology © 2014 Asian Pacific Society of Nephrology, 19 (Supp. 4), 89–97

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277 HYPERKALEMIA INDUCES FAILURE OF PACEMAKER FUNCTION IN HEMODIALYSIS PATIENT N AUNG, S MAY Tamworth Base Hospital, New South Wales, Australia Background: Hyperkalemia may cause cardiac pacemaker malfunctioning due to a reduction of the electronegativity of the resting myocardial potential. Both sensing and capture mechanisms could be temporarily affected, with possible life-threatening effects. Case Report: Mr. DT, 50 years old male with background history of End Stage Renal Failure due to diabetic nephropathy on maintenance hemodialysis, Aortic Valve Replacement, Pacemaker for third degree AV block presented to ED in a small rural hospital with lethargy and unwell. BP 82/50 mmHg, HR 22/min. ECG showed significant bradycardia 20/min with failure of rhythm to capture the pacing. Arrangement was made for urgent transfer to Metropolitan unit with pacemaker malfunction. Subsequent result: K 7.6 mmol, BSL 52.8 mmol. Repeat ECG show similar finding with no classic hyperkalemia changes. Patient was treated with usual medications for hyperkalemia and commenced on insulin infusion. At the same time, Haemodialysis was commenced. After 30 minutes on dialysis, patient’s vital sign improved to BP 100/70 mmHg, HR 65/min with ECG showing normal ventricular paced rhythm. Conclusions: Hyperkalemia is a cause of acute pacemaker malfunction without classical hyperkalemia ECG change due to a failure of pacemaker sensing and capturing. Acute treatment of hyperkalemia will restore pacemaker function.

278 ALLERGIC INTERSTITIAL NEPHRITIS FOLLOWING PROTON PUMP INHIBITOR and H2 RECEPTOR ANTAGONIST ADMINISTRATION C GARCIA1, P COLEMAN2 1 Hornsby Ku-ring-gai Hospital, Sydney, NSW; 2Manly Hospital, Sydney, NSW, Australia Background: We report a case of acute interstitial nephritis (AIN) to a protonpump inhibitor (PPI) and H2 receptor antagonists (H2RA) prescribed to treat gastro-oesophageal reflux disease (GORD). Case Report: A 56-year-old man was referred for investigation of nocturnal polydipsia and an elevated serum creatinine of 130 μmol/L. The patient’s history included GORD, hypertension and gout. The patient had no history of kidney disease or drug allergies. The patient’s medications consisted of Allopurinol 300 mg daily, Verapamil 180 mg daily, Meclobomide 600 mg daily and Perindopril 7.5 mg nocte. He had also been taking Omeprazole 20 mg mane for four years. PPI-induced AIN was suspected and the patient’s serum creatinine normalised to 80 μmol/L following the replacement of Omeprazole with Ranitidine 300 mg daily. The serum creatinine deteriorated to 175 μmol/L after the Omeprazole was reintroduced because of worsening symptoms of GORD but returned to 80 μmol/L after the Omeprazole was again replaced with Ranitidine. Six months later, whilst taking Ranitidine 300 mg daily, the serum creatinine unexpectedly deteriorated to 195 μmol/L and the patient developed a normochromic normocytic anaemia and sterile pyuria. A kidney biopsy confirmed a diagnosis of AIN. The Ranitidine was ceased and a four-week course of prednisolone was instituted. Four years later, the serum creatinine was 90 μmol/L. Deteriorating symptoms of GORD and concern regarding worsening oesophagitis prompted a trial of Famotidine 20 mg nocte. The serum creatinine promptly increased to 180 μmol/L and normalised following withdrawal of the Famotidine. Conclusions: As far as we are aware, this is the first reported case of AIN to both PPIs and H2RAs in a patient.

279 GRAM NEGATIVE SEPSIS POST RENAL TRANSPLANT BIOPSY IN PATIENT WITH ASYMPTOMATIC PYELONEPHRITIS H AL-KHAYYAT, N TOUSSAINT, S HOLT, P HUGHES Department of Nephrology, The Royal Melbourne Hospital, Parkville, Victoria, Australia Background: Pyelonephritis in patients post renal transplantation has a reported incidence between 10–25% and nearly half of cases are asymptomatic. Transplant

pyelonephritis shares many histopathological changes with cellular rejection (interstitial infiltrate, tubulitis) and may mask detection of rejection. Case Report: 41-year male with end-stage kidney disease secondary to IgA nephropathy (haemodialysis for 6 years) underwent a cadaveric renal transplant in 2004. Other medical history included hypertension, ischemic heart disease, and AF on warfarin. With worsening graft function after 10 years (Cr increased from 140 to 200 μmol/L) a renal biopsy was performed. The patient was asymptomatic and admitted the day before as he was rurally based. Pre-biopsy tests included urine microscopy which was pending at the time of the procedure. There were no immediate complications from the biopsy however after two hours the patient became febrile and developed rigors and hypotension. The patient also developed macroscopic haematuria with clot retention. CT abdomen revealed no haematoma. Empiric antibiotics were commenced. Blood cultures subsequently grew both Enterobactor and E. coli species and both were also cultured on the urine sample taken the day prior to the biopsy. The patient required ICU admission with inotropic support. He was discharged home after one week with renal function slightly better than on admission. Histopathology revealed active pyelonephritis on a background of severe tubular atrophy and interstitial fibrosis, although rejection could not be excluded as cause of graft dysfunction. Conclusion: We report a case of asymptomatic renal allograft pyelonephritis which developed into septicaemia following an indication renal biopsy for worsening renal function. Obstruction from haematuria may have contributed to the severity of the complication. Acute rejection as a cause of graft dysfunction was not able to be excluded. There are limited reports relating to the difficulties in differentiating pyelonephritis and cellular rejection in transplant recipients.

280 CEFEPIME RELATED INTERSTITIAL NEPHRITIS: A CASE REPORT K MAC, K HOWLIN, J WONG Department of Renal Medicine, Sydney South West Area Health Service, Australia Background: Cefepime is fourth-generation cephalosporin that is prescribed widely for severe infections varying from pyelonephritis to empirical therapy for febrile neutropenia. It is well tolerated and severe adverse events are uncommon. Reversible neurotoxicity regardless of dose adjustment for renal impairment has been reported. Here we report a case of acute kidney injury (AKI) due to severe tubulointerstitial nephritis associated with long-term use of cefepime for treatment of temporal bone osteomyelitis. Case Report: A 62-year-old female with normal renal function (creatinine 70 μmol/L) received intravenous cefepime for chronic osteomyelitis of the right temporal bone. She developed dysgeusia after 2 weeks and AKI with creatinine rising up to 300 μmol/L after 6 weeks of therapy. Her medical background included: diet controlled diabetic mellitus and well controlled hypertension. Urinalysis was bland. Autoimmune screen was negative. Renal biopsy confirmed tubulointerstitial nephritis. Corticosteroids were not administered given her diabetes, active infection, and prompt response to Cefepime discontinuation. She was continued on ciprofloxacin followed by oral amoxicillin. Her renal function improved but recovery remains incomplete at 6 months (creatinine 110 μmol/L). Conclusions: To our knowledge this is the first report of cefepime associated tubulointerstitial nephritis. Tubulointerstitial nephritis with cefepime neither relates to past or future beta lactam antibiotic exposure in spite of reported incidence of 10% cross sensitivity between penicillin-derivatives, cephalosporins and carbapenems. Awareness of this adverse event is important because of in increasing use of cefepime in the multi drug resistant era.

281 ATYPICAL PRESENTATION OF ANTI-GLOMERULAR BASEMENT MEMBRANE DISEASE WITH CO-EXISTING IgA NEPHROPATHY A LECAMWASAM1, A SKENE2, D LEE1, L MCMAHON1 1 Department of Renal Medicine, Eastern Health, Melbourne, Victoria; 2Department of Anatomical Pathology, Austin Health, Melbourne, Victoria, Australia Background: We report a case of atypical presentation of anti-glomerular basement membrane (anti-GBM) disease co-existing with IgA nephropathy. Case Report: A 56-year-old Caucasian normotensive man presented with prodromal symptoms for a month. Kidney function deteriorated over 3 weeks with serum creatinine from 134 to 194 μmol/L, while it was normal 14 months prior. Urine microscopy revealed microscopic haematuria but no red cell casts, and spot urine protein-to-creatinine ratio was 0.057 mg/mmol. Anti-GBM antibody titre was 57 units/mL (