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Acute renal failure in an AIDS patient on tenofovir: a case report
Pinelopi P Kapitsinou, Naheed Ansari
Journal of Medical Case Reports , 2008, DOI: 10.1186/1752-1947-2-94
Abstract: We report a patient who developed ARF and Fanconi syndrome during treatment with tenofovir. Despite severe metabolic acidosis associated with a creatinine of 9.8 mg/dL (866 μmol/L), this patient's condition improved on discontinuation of tenofovir treatment without requiring renal replacement therapy.Vigilant screening of kidney function is required regularly after initiation of tenofovir due to possible appearance of renal failure.Tenofovir is a nucleotide reverse-transcriptase inhibitor which was approved for use by the Food and Drug Administration in 2001 for the treatment of HIV. It belongs to the same class as adefovir and cidofovir which have well documented renal toxicities including proximal renal tubule cell dysfunction and acute renal failure (ARF) [1,2]. The described mechanism of tubular toxicity for the latter two drugs is cellular accumulation through increased entry from the hOAT (organic anion transporters located on the basolateral side of the tubule) and decreased efflux into tubular lumen mediated by the MRP 2 (Multidrug-Resistance-Protein) [3]. Similar effects were not expected with tenofovir due to decreased interaction with human organic transporter 1 and minimal mitochondrial toxicity in vitro [2,3].Twenty seven cases of tenofovir related tubular dysfunction and Fanconi syndrome have been described in the medical literature. We describe another case of a patient in whom ARF and Fanconi syndrome developed during treatment with tenofovir.A 53-year-old woman with AIDS of 6 years duration developed progressive weakness, dyspnea on exertion and constipation. Her symptoms also included decreased appetite, weight loss and episodes of lightheadness. She had a history of drug and alcohol addiction, seizure disorder, stroke, pancreatitis and chronic low back pain and she was known to have been Hepatitis B and C positive since 2002. Antiretroviral therapy, consisting of abacavir, lamivudine and zidovudine, had been started in March 2002, when she was fou
Tenofovir Renal Toxicity: Evaluation of Cohorts and Clinical Studies—Part One  [PDF]
Adikwu Elias, Ogbuehi Ijeoma, Nkereuwem Jonathan Edikpo, Deo Oputiri, Oru-Bo Precious Geoffrey
Pharmacology & Pharmacy (PP) , 2013, DOI: 10.4236/pp.2013.49092

Tenofovir is one of the most commonly used antiretrovirals in adolescents and adults because of its potency and favorable pharmacokinetic and relative safety toxicological profile. It has been combined successfully with antiretroviral drugs from classes such as protease inhibitors, non-nucleoside reverse transcriptase inhibitors and nucleoside reverse transcriptase inhibitors to achieve virologic suppression in a high percentage of recipients. Despite its therapeutic success, quite a number of cohorts and clinical studies have associated tenofovir with the development of renal toxicity with few studies on the opposing end. This stimulated us to review reported cohorts and clinical studies on tenofovir renal toxicity. In this study it was observed that literature reported incidence of tenofovir renal toxicity falls within the range of 0.7%-17%. Available studies gave different appellations to tenofovir renaltoxicity, which include fanconis syndrome, proximal tubule dysfunction, acute renal failure, chronic renal failure, chronic kidney disease and nephrogenic diabetes insipidus. Markers of renal toxicity (tubulopathy) which include glycosuria, hyperaminoaciduria, proteinuria, hyperphosphaturia, hyperuricosuria, retinol-binding protein, beta2-microglobulinuria, decreased creatinine clearance and

Renal failure due to primary amyloidosis: a case report and literature review
Mello, Ramon Andrade Bezerra de;Santos, Dania Sofia Neiva Marques;Freitas-Silva, Margarida Paula Rebelo Nunes;Andrade, Joaquim Aguiar;
Sao Paulo Medical Journal , 2011, DOI: 10.1590/S1516-31802011000300009
Abstract: context: primary amyloidosis, also known as al amyloidosis, is commonly caused by clonal expansion of plasma cells in the bone marrow, thereby segregating light chains of clonal immunoglobulin that settle in tissues in the form of insoluble amyloid fibrils. the aim of this study was to report a case of primary amyloidosis with renal failure, diagnosed in hospital s?o jo?o, porto, portugal, focusing on the diagnostic difficulties and presenting a literature review. case report: a 68-year-old caucasian man was admitted to the internal medicine department of the hospital with a condition of anasarca and nephrotic syndrome. after performing a renal biopsy that tested positive using congo red and immunohistochemistry, lambda light chain amyloidosis was diagnosed. this evolved into terminal renal disease, which led to hemodialysis and several episodes of urinary and catheter infections. he was started on chemotherapy, consisting of bortezomib 0.7 mg/m2 and dexamethasone 40 mg in six cycles. this led to clinical improvement, stabilization of the illness and good tolerance of the treatment. conclusion: amyloidosis is a rare entity that is difficult to diagnose. this is because of the unspecific early clinical manifestations of the disease. the hypothesis of amyloidosis is only considered when specific organ failure occurs. this case consisted of primary amyloidosis with involvement of the kidneys as an initial presentation of the disease and its difficulties were shown, going from the clinical approach to the final diagnosis.
A Mouse Model of Early-Onset Renal Failure Due to a Xanthine Dehydrogenase Nonsense Mutation  [PDF]
Sian E. Piret, Christopher T. Esapa, Caroline M. Gorvin, Rosie Head, Nellie Y. Loh, Olivier Devuyst, Gethin Thomas, Steve D. M. Brown, Matthew Brown, Peter Croucher, Roger Cox, Rajesh V. Thakker
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045217
Abstract: Chronic kidney disease (CKD) is characterized by renal fibrosis that can lead to end-stage renal failure, and studies have supported a strong genetic influence on the risk of developing CKD. However, investigations of the underlying molecular mechanisms are hampered by the lack of suitable hereditary models in animals. We therefore sought to establish hereditary mouse models for CKD and renal fibrosis by investigating mice treated with the chemical mutagen N-ethyl-N-nitrosourea, and identified a mouse with autosomal recessive renal failure, designated RENF. Three-week old RENF mice were smaller than their littermates, whereas at birth they had been of similar size. RENF mice, at 4-weeks of age, had elevated concentrations of plasma urea and creatinine, indicating renal failure, which was associated with small and irregularly shaped kidneys. Genetic studies using DNA from 10 affected mice and 91 single nucleotide polymorphisms mapped the Renf locus to a 5.8Mbp region on chromosome 17E1.3. DNA sequencing of the xanthine dehydrogenase (Xdh) gene revealed a nonsense mutation at codon 26 that co-segregated with affected RENF mice. The Xdh mutation resulted in loss of hepatic XDH and renal Cyclooxygenase-2 (COX-2) expression. XDH mutations in man cause xanthinuria with undetectable plasma uric acid levels and three RENF mice had plasma uric acid levels below the limit of detection. Histological analysis of RENF kidney sections revealed abnormal arrangement of glomeruli, intratubular casts, cellular infiltration in the interstitial space, and interstitial fibrosis. TUNEL analysis of RENF kidney sections showed extensive apoptosis predominantly affecting the tubules. Thus, we have established a mouse model for autosomal recessive early-onset renal failure due to a nonsense mutation in Xdh that is a model for xanthinuria in man. This mouse model could help to increase our understanding of the molecular mechanisms associated with renal fibrosis and the specific roles of XDH and uric acid.
Silent onset of postmenopausal endometriosis in a woman with renal failure in hormone replacement therapy: a case report
Ugo Indraccolo, Fabrizio Barbieri
Journal of Medical Case Reports , 2010, DOI: 10.1186/1752-1947-4-248
Abstract: We present the case of a 54-year-old Italian Caucasian woman in surgical menopause with a history of ovarian endometriosis, who underwent voluntary hormone replacement therapy for seven years. She developed postrenal renal failure due to bilateral compression of the pelvic ureteral tract caused by two large, deeply infiltrating endometriotic nodules with no pelvic pain. She underwent operative laparoscopy with adhesiolysis of enteroenteric adhesions and excision of the endometriotic nodules encompassing the juxtavesical tract of the ureters, without obtaining improvement of renal failure.Postmenopausal endometriosis can manifest itself in an unpredictable and potentially very serious manner. It is therefore important to carefully evaluate the risks and benefits of administering hormone replacement therapy to patients with previous endometriosis.Postmenopausal endometriosis is a rare form of a common disease, given that the absence of estrogenic hormone production should halt disease progression [1]. Oxholm et al [2] reported that two to five percent of endometriosis is diagnosed after menopause. It has been reported that endometriosis may develop essentially in women undergoing hormone replacement therapy [2] with some exceptions [3], indicating the possibility that in some cases endometriosis may be completely independent of gonadic estrogens. Whether postmenopausal endometriosis is due to exogenous estrogens or presumably independent of gonadic estrogens, the silent growth of the disease can result in potentially serious and unpredictable complications. For example, it may grow without the typical symptoms such as catamenial pain and may involve the ureters [4,5] or bowel [6], producing complications such as renal failure or intestinal obstruction. The following case explains the onset of postmenopausal endometriosis with renal failure.A 54-year-old Italian Caucasian woman, weighing 71 kg and with a height of 160 cm, was admitted to our facility in order to have a
The effect of low serum bicarbonate values on the onset of action of local anesthesia with vertical infraclavicular brachial plexus block in patients with End-stage renal failure  [cached]
Al-mustafa Mahmoud,Massad Islam,Alsmady Moaath,Al-qudah Abdullah
Saudi Journal of Kidney Diseases and Transplantation , 2010,
Abstract: Vertical infraclavicular brachial plexus block is utilized in patients with chronic renal failure at the time of creation of an arterio-venous fistula (AVF). The aim of this study is to test the effect of impaired renal function, with the resulting deranged serum electrolytes and blood gases, on the success rate and the onset of action of the local anesthetics used. In this prospective clinical study, we investigated the effect of the serum levels of sodium, potassium, urea, crea-tinine, pH, and bicarbonate on the onset of action of a mixture of lidocaine and bupivacaine administered to create infraclavicular brachial plexus block. A total of 31 patients were studied. The success rate of the block was 93.5 % (29 patients). The mean onset time for impaired or re-duced sensation was found to be 8.9 ± 4.7 mins and for complete loss of sensation, was 21.2 ± 6.7 mins. There was no significant association with serum sodium, potassium, urea, creatinine or the blood pH level (P> 0.05). The bivariate correlation between serum bicarbonate level and the partial and complete sensory loss was -0.714 and -0.433 respectively, with significant correlation (P= 0.00, 0.019). Our study suggests that infraclavicular block in patients with chronic renal failure carries a high success rate; the onset of the block is delayed in patients with low serum bicarbonate levels.
Tenofovir Renal Toxicity: Evaluation of Cohorts and Clinical Studies—Part 2  [PDF]
Adikwu Elias, Ogbuehi Ijeoma, Nkereuwen Jonathan Edikpo, Deo Oputiri, Oru-Bo Precious Geoffrey
Pharmacology & Pharmacy (PP) , 2014, DOI: 10.4236/pp.2014.51015

Tenofovir is a nucleotide reverse transcriptase inhibitor used as part of antiretroviral regimens. It is well tolerated with relative toxicological effects but recent reports have linked it with renal toxicity which is of clinical concern. This study reviews literary work on tenofovir renal toxicity with more light on case reports. Tenofovir renal toxicity manifests as Fanconi’s syndrome, nephrogenic diabetes insipidus and acute renal failure. Fanconi’s syndrome is characterised by acidosis, protenuria, albuminuria, aminoaciduria, hyperchloremic, metabolic acidosis, hypouricemia, hypophosphatemia and glycosuria. The presence of urine osmolality, polydipsia and polyuria could give credence totenofovir induced nephrogenic diabetes insipidus. In some cases of tenofovir renal toxicity, renal biopsy revealed sclerosed glomeruli with ischemic injury including portal collapse of capillary loops. Histopathological changes in glumeruli include mild mesangial proliferation, increased mesangial matrix and thickened capillary loops. Moderate degenerative tubular changes, loss of tubular mass, interstitial scarring and scattered cellular infiltrates. Pharmacodynamic and pharmacokinetic interactions may occur with the co administration of tenofovir with non steroidal anti-inflammatory drugs, aminoglycosides and some protease inhibitors which may potentiate renal toxicity. Tenofovir renal toxicity is associated with some risk factors including genetic polymorphism as supported by dichotomy in renal toxicity among different race and the association between ABCC2 gene and tenofovir kidney tubular dysfunction. The pharmacology of tenofovir renal toxicity is unclear but it is attributed to the interaction between tenofovir and theorganic anion transporters (hOAT1, and to a lesser extent, OAT3) favoring intracellular accumulation in renal proximal tubule cells. This may lead to ultrastructural mitochondrial abnormalities and decreased mtDNA levels which could stimulate reactive oxygen species production, depletion of antioxidants and antioxidant enzymes. These

Concurrent nephrotic syndrome and acute renal failure caused by chronic lymphocytic leukemia (CLL): a case report and literature review
Xianrui Dou, Haitang Hu, Yongle Ju, Yongdong Liu, Kaifu Kang, Shufeng Zhou, Wenfang Chen
Diagnostic Pathology , 2011, DOI: 10.1186/1746-1596-6-99
Abstract: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2479639195566762 webcite.AL amyloidosis is characterized by widespread, progressive deposition of amyloid fibrils derived from monoclonal immunoglobulin (Ig) light chains, leading to multi-system organ failure among which the kidneys and heart are most frequently affected [1]. Although AL amyloidosis is typically caused by plasma cell proliferative disease especially multiple myeloma, it can also be caused by other lymphoproliferative disorders of B-cells such as lymphoplasmacytic lymphoma, of which the neoplastic B cells produce monoclonal immunoglobulin light chains [2]. Only few cases of AL amyloidosis associated with chronic lymphocytic leukemia (CLL) have been reported [2-5]. Another relatively common injury caused CLL is the direct neoplastic cell infiltration as demonstrated by autopsy studies [6], but acute renal failure due to severe infiltration is rare [7-9].In this report, we present a patient with nephrotic syndrome and renal failure associated with CLL. The patient completely recovered from the nephrotic syndrome and renal dysfunction after CLL was controlled with chemotherapy. We have reviewed the literature and discussed the relationship between CLL and amyloidosis and the pathological implications.A 54-year-old male Chinese patient was admitted to the Shunde People's hospital on March 7, 2008, complaining of nocturia and edema of face and both lower extremities for more than two months. The patient had no history of any renal disease. Physical examinations revealed normal vital signs, moderate hypertension (162/96 mmHg) and pitting edema of the lower extremities. Enlargement of lymph nodes involving inguinal, axillary, submaxillary and supraclavicular fossa with a diameter of more than 1 cm was found. The remainder of the examination was unremarkable.Both his hemoglobin and erythrocyte count were in normal range. The leukocytes increased to 16.8 ×
Ultra late onset group B streptococcal sepsis with acute renal failure in a child with urethral obstruction: a case report
Daniela Freudenstein, Konrad Reinshagen, Angela Petzold, Angelika Debus, Horst Schroten, Tobias Tenenbaum
Journal of Medical Case Reports , 2012, DOI: 10.1186/1752-1947-6-68
Abstract: We present a rare case of a five-month-old Caucasian boy with ultra late onset urosepsis and acute renal failure caused by group B streptococci serotype V. Excretion urography showed a subvesical obstruction that consequently was surgically corrected after antibiotic treatment of the acute infection.Group B streptococci serotype V, urogenitary tract malformations, previous hospitalization and medical interventions may be important risk factors for the development of ultra late onset Group B streptococci sepsis in non-neonates.Group B Streptococcus (GBS) is a leading cause of infection in newborns, pregnant women, and older persons with chronic medical illness. Cervicovaginal colonization with GBS in pregnant women can result in vertical transmission of GBS to neonates, with a limited number of GBS capsular serotypes being disproportionately associated with colonization and disease; serotypes Ia, III, and V, for example, cause the majority of invasive infections in older persons [1]. Multiple serotypes of GBS also cause urinary tract infections (UTIs), which encompass asymptomatic bacteriuria, cystitis, pyelonephritis, urethritis, and urosepsis [1,2]. GBS asymptomatic bacteriuria is particularly common among pregnant women; however, those most at risk for cystitis due to GBS are older persons and immunocompromised individuals [2,3]. Predisposing factors for GBS UTI may include diabetes mellitus and chronic renal failure [4].A critically ill five-month-old Caucasian boy presented with a four-day history of fever of unknown origin up to 39°C at our hospital. One week prior to the current admission he had undergone herniotomy and orchidopexy and was discharged after two days. During this hospital admission a distended bladder had been observed after herniotomy and the child was subsequently catheterized. The catheterization was described as uneventful; therefore, no further diagnostics were initiated. On the current admission, the child appeared septic without inflammat
Acute Renal Failure and Jaundice without Methemoglobinemia in a Patient with Phenazopyridine Overdose: Case Report and Review of the Literature  [PDF]
Ian Holmes,Nathaniel Berman,Vinicius Domingues
Case Reports in Nephrology , 2014, DOI: 10.1155/2014/845372
Abstract: Phenazopyridine is a commonly used urinary analgesic available throughout the United States. Ingestion of large quantities can lead to methemoglobinemia, hemolytic anemia, jaundice, and acute renal failure. We report a case of a 78-year-old male with previously normal renal function who developed acute renal failure and jaundice without methemoglobinemia or hyperbilirubinemia after taking nearly 8?g of phenazopyridine over the course of 4 days. Initially presenting with oliguria, the urine output began to increase by day 2 of his admission, and the creatinine peaked 11 days after he began taking phenazopyridine, and he was discharged safely soon after. To our knowledge, this is the first such case of renal failure and jaundice without methemoglobinemia or hemolytic anemia in an adult patient with normal renal function. 1. Introduction Phenazopyridine is a commonly prescribed urinary analgesic which has been in use since the 1920s [1]. Its use is associated with gastrointestinal discomfort and orange discoloration of urine [2]. Rarely, patients have developed pigment stones due to the red azo dye which is part of the drug’s formulation [1]. In large doses, phenazopyridine has been reported to cause renal failure, methemoglobinemia, skin pigmentation, and hemolytic anemia [2–7]. These findings often occur together, although isolated renal failure has been reported in pediatric patients and in patients with underlying renal disease [4, 7, 8]. We report a case of anuric renal failure and jaundice due to phenazopyridine without hyperbilirubinemia, methemoglobinemia, or hemolytic anemia in a patient without underlying renal disease. Previous case reports of phenazopyridine-associated kidney injury have either been in pediatric patients or in patients with underlying renal disease; to our knowledge, this is the first such case in a patient with normal renal function [3]. 2. Case Report A 78-year-old male physician with no prior renal disease presented to the emergency department with anuria. Five days prior to presentation, he had developed dysuria and urinary frequency and started himself on levofloxacin and phenazopyridine. Over the course of four days, he had taken 39 200?mg tabs of phenazopyridine (approximately 7.8?g). One day prior to admission, he noted that his urine output had ceased despite increased oral intake and decided to present to the emergency department. On presentation, the patient was hypotensive to 70/40 with a heart rate of 91?bpm but had no orthostatic symptoms. He received four liters of normal saline with no improvement in urine
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