[Bilateral renal papillary necrosis of spontaneous resolution as a cause of microscopic hematuria. Report of one case]. / Necrosis papilar renal bilateral de resolución espontánea como causa de hematuria microscópica. Caso clínico.

Renal papillary necrosis is an infrequent cause of hematuria characterized by ischemic necrosis of the renal medulla, especially the papilla. Its most common cause is analgesic abuse. Despite being oligo-symptomatic, in many cases its presence is associated with serious functional sequelae. Imaging, especially computed tomography, is essential to make the diagnosis. We report a 63-year-old female studied for an asymptomatic microscopic hematuria whose tomographic study showed a bilateral renal papillary necrosis. No etiology was found, and she evolved with a spontaneous complete remission.

Prevalence and associations of symptomatic renal papillary necrosis in sickle cell anemia patients in South-Eastern Nigeria.

AIM: To assess the prevalence and associations of symptomatic renal papillary necrosis (RPN) in sickle cell anemia patients. PATIENTS AND METHODS: The case notes of homozygous hemoglobin (Hb) S patients diagnosed with RPN were retrospectively assessed. Diagnosis was based on microscopic hematuria and positive ultrasound findings. Their steady state diastolic blood pressure, Hb, leukocyte count, platelet count, serum direct bilirubin, and aspartate transaminase, were obtained by automated analyzers. These were evaluated for any relationship with the occurrence of RPN. RESULTS: Two hundred and twenty patients were assessed aged 6-55 years with a median age of 24 years. The prevalence of symptomatic RPN was found to be 2.3%. RPN was positively associated with the female gender (Chi-square P value 0.001), but not with any other clinical or laboratory variable. However, other predictors of disease severity were positively associated with RPN such as age, diastolic blood pressure 0.180 (P = 0.016), serum aspartate transaminase, serum bilirubin 0.145 (0.027), Hb, and leukocyte count - 0.155 (P = 0.003). CONCLUSION: The prevalence of symptomatic RPN is low in this group of homozygous S patients and occurs more commonly in females. Improvement in care for these patients will reduce these chronic complications.

Severe anemia in an adolescent male with sickle cell trait: a case report.

BACKGROUND: Sickle cell trait is generally considered a benign condition. However, it has been associated with uncommon comorbidities such as painless gross hematuria secondary to renal papillary necrosis and renal medullary carcinoma. OBSERVATION: We present a 16-year-old African American boy with sickle cell trait and a recent history of prolonged gross hematuria due to renal papillary necrosis. The patient developed severe iron deficiency anemia and required transfusion support. CONCLUSIONS: Although renal papillary necrosis is well-described, it is uncommon in pediatrics and only rarely results in the need for transfusion.

Renal candidiasis associated with papillary necrosis in a captive tiger (Panthera tigris).

A 14-year-old male tiger developed anorexia with elevated blood urea nitrogen and creatinine levels. The patient had a palpable abdominal mass and demonstrated neutrophilic leukocytosis and anaemia. Leukocytes, yeast and bacteria were present in the urine. The animal was non-responsive to therapy and was subsequently euthanised. Extensive acute renal papillary necrosis (RPN) with pyelonephritis, chronic nephritis and polycystic renal disease were evident during gross and microscopic pathology examinations. The histologic occurrence of fungal spores and pseudohyphae morphologically consistent with Candida species were observed within the necrotic papillary regions of the kidney and within multiple foci of mild parakeratotic hyperkeratosis present in the gingiva and tongue. Candida albicans along with a slight growth of Escherichia coli were recovered from kidney cultures. Possible contributory factors for the renal candidiasis and associated RPN include predisposing oral candidiasis, polycystic renal disease, ischaemic nephrosclerosis, age-associated or other forms of immunodeficiency and therapy with meloxicam, a non-steroidal anti-inflammatory drug. The absence of apparent lower urinary tract involvement coupled with the presence of intravascular renal 'Candida emboli' suggest that chronic oral candidiasis was the probable source of the kidney infection.

Candidal renal papillary necrosis conquered.

Renal papillary necrosis due to Candida albicans is a rare but treatable cause of acute renal failure. We report this case of a middle aged male with history of type 2 diabetes mellitus who presented with infected right lower extremity and right lower lobe pneumonitis with hypotension. Though, he improved initially, during his stay in the hospital, he developed acute renal failure. Blood culture grew Candida albicans and the renal biopsy revealed candidal renal papillary necrosis. He also had candidal retinitis on ophthalmoscopy examination. He was treated with parenteral fluconazole for two weeks followed by oral fluconazole for a total of 4 weeks. Following treatment, the patient improved symptomatically and his renal parameters returned to normal. This case illustrates the need to consider candidal papillary necrosis as a differential in an immunocompromised patient with acute renal failure. It is potentially reversible, nonetheless a diagnostic and therapeutic challenge.

Identification and regulation of reticulon 4B (Nogo-B) in renal tubular epithelial cells.

Nogo-B is a member of the reticulon family of proteins that has been implicated in diverse forms of vascular injury. Although Nogo-B is expressed in renal tissues, its localization and function in the kidney have not been examined. Here, we report that Nogo-B is expressed specifically in the epithelial cells of the distal nephron segments in the murine kidney. After unilateral ureteral obstruction (UUO) and ischemia/reperfusion, Nogo-B gene and protein levels increased dramatically in the kidney. This increase was driven in part by injury-induced de novo expression in proximal tubules. Examination of Nogo-B immunostaining in human biopsy specimens from patients with acute tubular necrosis showed similar increases in Nogo-B in cortical tubules. Mice genetically deficient in Nogo-A/B were indistinguishable from wild-type (WT) mice based on histological appearance and serum analyses. After UUO, there was a significant delay in recruitment of macrophages to the kidney in the Nogo-A/B-deficient mice. However, measurements of fibrosis, inflammatory gene expression, and histological damage were not significantly different from WT mice. Thus, Nogo-B is highly expressed in murine kidneys in response to experimental injuries and may serve as a marker of diverse forms of renal injury in tissues from mice and humans. Furthermore, Nogo-B may regulate macrophage recruitment after UUO, although it does not greatly affect the degree of tissue injury or fibrosis in this model.

[Intracranial hypertension and lupus]. / Hypertension intracrânienne et lupus.

INTRODUCTION: Idiopathic intracranial hypertension (IH) occurs most commonly in women and overweight subjects. It must be reported associated to general diseases, like systemic lupus erythematosus (SLE). METHODS: We report an observation of a patient with lupus complicated by glomerulonephritis and IH. OBSERVATION: A 29 years old woman, without overweight, was followed for a SLE with skin and arthritic involvement . Four years after onset, a renal complication appeared with severe nephrotic syndrome. Six weeks after, bilateral papillar oedema was discovered, revealing an IH, as the patient was treated by oral steroids at 1mg/kg/d and bimonthly intravenous cyclophosphamide. The patient was completely asymptomatic. Brain MRI with veino-RMN was normal, without cerebral venous thrombosis. Lumbar punction showed an elevated opening pressure of 30,5 cmH(2)0 but with normal cerebrospinal fluid (CSF) contents. Evacuation of 30 mL of CSF and immunosuppressive treatment allowed symptoms regression. DISCUSSION/CONCLUSION: Twenty-seven cases of IH associated to SLE with nephritis have been reported in literature. Young women are more frequently involved with in half of cases a diffuse proliferative glomerulonephritis. Predisposing factors, like anaemia, must be associated. IH allows SLE diagnose in more than the third of the cases. Then, SLE has to be searched as an etiology of IH, in particular in non-obese patients and when nephritis is associated.

Application of Dolichos biflorus in immunoassay detection of kidney collecting duct biomarkers.

Currently there are no biomarkers for detecting collecting duct damage in man. Antibodies to several collecting duct-specific antigens exist but sandwich assays have been difficult to establish due to the need for two different antibodies to the same protein. We hypothesized that a collecting duct-specific lectin could be used in combination with a collecting duct-specific antibody to negate the need for two different antibodies. The collecting duct specificity of selected antibodies (NiCa II 13C2, Pap XI 3C7, HuPaP VII 2B11 and aquaporin 2), was verified by immunohistochemistry. Aquaporin 2 and Pap XI 3C7 were used successfully in setting up assays with the lectin Dolichos biflorus, using the Meso Scale Discovery (MSD) platform. Antigen expression was highest in the papillae of rat and human kidney (corresponding to the greatest density of collecting ducts) and was also present in normal urine. We propose that further qualification and validation would lead to an assay for detecting collecting duct damage in man.

Low dose, oral epsilon aminocaproic acid for renal papillary necrosis and massive hemorrhage in hemoglobin SC disease.

Renal papillary necrosis in sickling hemoglobinopathies can lead to significant complications, including hemorrhage, obstruction, and infection. Despite its frequency, there are limited therapies for protracted hemorrhage. In the past, massive hemorrhage was managed with nephrectomy. Here, we report a patient with hemoglobin SC disease and prolonged, life-threatening hemorrhage from papillary necrosis successfully treated with oral, low-dose epsilon aminocaproic acid (EACA). Although further study is warranted, this case illustrates the need to consider EACA in the conservative management of renal papillary necrosis and significant hemorrhage in sickle cell hemoglobinopathies.

Characterization of renal papillary antigen 1 (RPA-1), a biomarker of renal papillary necrosis.

Renal papillary necrosis (RPN) is a relatively common toxicity observed in preclinical drug safety testing. It is also observed in a variety of human diseases. RPN is difficult to diagnose without expensive scanning methods or histopathology. A noninvasive biomarker that could be detected at early stages of kidney damage would be of great value both to preclinical drug safety testing and in the clinic. An antibody raised to an unknown epitope of an antigen in rat kidney papilla was found to be specific for collecting duct cells in the kidney; this was termed renal papillary antigen 1 (RPA-1). In this study, the authors show that RPA-1 is an early biomarker of RPN in two different rat models of toxicity: 2-bromoethanamine (BEA) and N-phenylanthranilic acid (NPAA). RPA-1 can be detected in urine at early stages of toxicity and correlates well with the histopathology observed. We also characterized the biochemical properties of RPA-1 and found that the antigen is a high molecular weight membrane bound glycoprotein, with the epitope likely to be carried on an N-linked carbohydrate structure. This study demonstrates that RPA-1 is an excellent marker of RPN that can be used to detect this toxicity in preclinical safety testing.

Over-the-counter analgesic use.

Chronic analgesic nephropathy, particularly chronic interstitial nephritis and renal papillary necrosis, results from daily use for many years of mixtures containing at least two analgesics and caffeine or dependence-inducing drugs. Computed tomography scan can accurately diagnose this disease even in the absence of reliable information on previous analgesic use. The occasion to moderate regular use of aspirin and nonsteroidal anti-inflammatory drugs is without renal risk when renal function is normal. Paracetamol use is less clear although the risk is not great. The continued use of non-phenacetin-combined analgesics with or without nonsteroidal anti-inflammatory drugs is associated with faster progression toward renal impairment. As long as high-risk analgesic mixtures are available over the counter, analgesic nephropathy will continue to be a problem.

Bilateral ureteric obstruction secondary to renal papillary necrosis.

A 2-year-old male presented to hospital with a 5-day history of vomiting and pyrexia. He was initially treated with non-steroidal medication as an anti-pyretic. Initial investigations demonstrated a raised urea and creatinine and he was treated with intravenous fluids. Within 24 h he became anuric with progressive renal insufficiency. Ultrasound scan demonstrated minimal bilateral hydronephrosis with debris in the lower pole calyces. The bladder was empty. Cystoscopy and retrograde contrast imaging revealed bilateral ureteric obstruction. Double J stents were inserted and his renal function returned to normal within 4 days. We believe the aetiology to be renal papillary necrosis and bilateral ureteric obstruction secondary to the administration of ibuprofen in association with dehydration.

[Sickle cell trait complications: A case series of 6 patients]. / Complications du trait drépanocytaire : à propos d'une série de 6 cas.

INTRODUCTION: Patients with sickle cell trait (SCT) are commonly considered as asymptomatic carriers. However, some clinical manifestations may occur. METHODS: Here we present a retrospective descriptive study about SCT subjects with at least one complication diagnosed in a sickle cell disease referral center, in Paris, between 2008 and 2019. We also performed a literature review on the complications of SCT subjects. RESULTS: Six patients (between 19 and 65 years old) were included. SCT was already known only for 4 of them at the time of the complication. Four patients presented with a splenic infarct after a stay in high altitude or a plane trip, one of them was associated with papillary necrosis; one patient had isolated papillary necrosis, and the last one had splenic sequestration. These complications happened for most of them after exposure to an unusual situation of hypoxia or deshydratation. Five out of 6 patients had a marked elevated C reactive protein. CONCLUSION: SCT may cause acute ischemic complications in a context of prolonged hypoxia or dehydration. The most commonly reported are the splenic infarct and the renal papillary necrosis. A study of hemoglobin should be considered in these clinical situations in patients with compatible ethnic origin.