A limited outbreak of nephropathogenic infectious bronchitis (NIB) occurred in three Delmarva (DMV) commercial broiler chicken flocks in 2011. Isolates of NIB virus (NIBV)--DMV/1639/11, DMV/3432/11, and DMV/3902/11--were characterized by sequence analysis of the N-terminal subunit (S1) of the spike (S) gene. Findings indicated that the isolates were identical to each other and to PA/9579A/10, a 2010 isolate from poultry in Pennsylvania. The 2010 and 2011 isolates appear to have originated from a 1997-2000 NIB outbreak in Pennsylvania. DMV/1639/11 and PA/9579A/10 were determined to be nephropathogenic in susceptible chickens, yielding virus reisolations from kidney and inducing characteristic interstitial nephritis microscopic lesions. In a controlled laboratory study, 40% of chickens vaccinated with a combination live vaccine containing infectious bronchitis virus (IBV) strains Massachusetts (Mass) + Connecticut (Conn) were positive on virus isolation attempts after challenge with DMV/1639/11, compared with only 13% of Mass + Arkansas (Ark) vaccinates. Both combination vaccines gave partial protection against the development of DMV/1639/11-induced renal lesions. Although numerically fewer chickens vaccinated with Mass + Conn had interstitial nephritis compared with those vaccinated with Mass + Ark, neither vaccine combination offered greater protection (P < 0.05) than observed in unvaccinated chickens challenged with DMV/1639/11. Mass + Ark vaccinations, applied under commercial conditions in the hatchery (spray) and on-farm (spray), did not protect the trachea or kidney from DMV/1639/11 challenge. Serologic testing of broiler flocks found < 3% (2 of 69) tested to possess specific antibodies to DMV/1639/11, indicating the virus had not become established in the region.

Transforming growth factor β1 (TGF-β1) is a cytokine involved in the process of pathological tissue sclerosis, which is part of the pathophysiological mechanism of end stage renal disease development. The aim of the study was to evaluate the association of the single nucleotide polymorphism rs1800471 of the TGFB1 gene with chronic kidney disease (CKD) occurrence and progression as well as hypertension appearance.It was a case-control study where 109 patients with CKD and 111 very old people were enrolled. The association of the studied polymorphism with mentioned diseases was assessed in the whole study group as well as in the subgroups stratified according to the underlying etiology of CKD: nephropathy in type 1 diabetes (n = 13), chronic glomerulonephritis (n = 50) and chronic interstitial nephritis (n = 46).No association of CKD progression with rs1800471 polymorphism was observed. The C allele was identified as the one associated with higher risk of the disease occurrence in the dominant model of inheritance (p = 0.035). The C allele in women, opposite to male gender, was associated with higher risk of CKD development (p = 0.038). GG genotype was associated with elevated risk of hypertension appearance (p = 0,0021).Due to the lack of accordance with previously performed studies it is still impossible to state an unequivocal conclusion regarding the association between rs1800471 polymorphism of the TGFB1 gene and risk of CKD occurrence and progression as well as hypertension appearance. That is why it is necessary to perform further studies in this field.

Adenine overload promotes intratubular crystal precipitation and interstitial nephritis. We showed recently that these abnormalities are strongly attenuated in mice knockout for toll-like receptors-2, -4, MyD88, ASC or caspase-1. We now investigated whether NF-κB activation also plays a pathogenic role in this model. Adult male Munich-Wistar rats were distributed among three groups: C (n = 17), receiving standard chow; ADE (N = 17), given adenine in the chow at 0.7% for 1 week and 0.5% for 2 weeks; and ADE+PDTC (N = 14), receiving adenine as above and the NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), 120 mg/kg/day in drinking water. After 3 weeks, widespread crystal deposition was seen in tubular lumina and in the renal interstitium, along with granuloma formation, collagen accumulation, intense tubulointerstitial proliferation and increased interstitial expression of inflammatory mediators. Part of the crystals was segregated from tubular lumina by a newly formed cell layer and, at more advanced stages, appeared to be extruded to the interstitium. p65 nuclear translocation and IKK-α increased abundance indicated activation of the NF-κB system. PDTC treatment prevented p65 migration and normalized IKK-α, limited crystal shift to the interstitium and strongly attenuated interstitial fibrosis/inflammation. These findings indicate that the complex inflammatory phenomena associated with this model depend, at least in part, on NF-κB activation, and suggest that the NF-κB system may become a therapeutic target in the treatment of chronic kidney disease.

BACKGROUND:

The association between sarcoidosis and glomerular diseases has not been extensively investigated in a large series and the potential features of this uncommon association remain to be determined.

METHODS:

We retrospectively identified 26 patients with biopsy-proven glomerular lesions that occurred in a sarcoidosis context. Potential remission of glomerular disease and sarcoidosis under specific treatment (steroid and/or immunosuppressive agents) was recorded for all patients. Demographic, clinical and biological characteristics were assessed at the time of kidney biopsy for each patient. Therapeutic data were analyzed for all patients.

RESULTS:

Glomerular disease occurred after the diagnosis of sarcoidosis in 11 of 26 cases (42%) (mean delay of 9.7 years). In six patients (23%), the glomerulopathy preceded the sarcoidosis diagnosis (mean delay 8 years). In the last nine patients (35%), both conditions occurred simultaneously. The most frequent glomerular disease occurring in sarcoidosis patients was membranous nephropathy in eleven cases. Other glomerular lesions included IgA nephropathy in six cases, focal segmental glomerulosclerosis in four patients, minimal change nephrotic syndrome for three patients and proliferative lupus nephritis in two patients. Granulomatous interstitial nephritis was associated with glomerular disease in six patients and was exclusively found in patients in whom the both disease occurred simultaneously. In nine patients with simultaneous glomerular and sarcoidosis diseases, we observed a strong dissociation between glomerular disease and sarcoidosis in terms of steroid responsiveness. At the end of the follow-up (mean of 8.4 years), six patients had reached end-stage renal disease and three patients had died.

CONCLUSIONS:

A wide spectrum of glomerular lesions is associated with sarcoidosis. The close temporal relationship observed in some patients suggests common causative molecular mechanisms of glomerular injury but complete remission of both diseases in response to exclusive steroid therapy is infrequent.

A 33-year-old man was diagnosed with Crohn's disease in 2001, and treated with mesalazine and ranitidine. Administration of infliximab was started in 2007 and led to a decrease in the activity of the Crohn's disease. He was referred to our department in the summer of 2011 following rapid progression of renal insufficiency, with serum creatinine levels increasing from 1.5 mg/dL to 4.3 mg/dL within 2 months. On admission, laboratory findings showed signs of inflammation, anemia, proteinuria, and hematuria. Renal biopsy results indicated the diagnosis of granulomatous interstitial nephritis. Neither clinical manifestations nor laboratory findings were suggestive of infectious disease, sarcoidosis, Wegener's granulomatosis or tubulointerstitial nephritis and uveitis. Mesalazine and ranitidine were discontinued in view of reports of drug-induced granulomatous interstitial nephritis. Levels of C-reactive protein immediately decreased, but renal function remained unimproved. Treatment with steroid pulse therapy was then initiated, followed by oral prednisolone at 40 mg/day, and his serum creatinine recovered to 2.3 mg/dL. Mesalazine and/or ranitidine appear to have been responsible for the granulomatous interstitial nephritis. In cases of Crohn's disease showing rapid deterioration of renal function, drug-induced renal disease should be considered, even if the drugs have been taken without apparent problems for a long duration.

Herbal therapies gained much popularity among the general public, but compared to therapies approved by official authorities, toxicological studies are frequently not available for them. Hence, there may be inherent risks and the kidneys may be especially vulnerable to toxic effects. Herbs may induce nephrotoxicity by induction of apoptosis. High oxalate contents in Star fruit (Averrhoa carambola L.) may induce acute nephropathy. Triptolide from Thunder God Vine (Triperygium wilfordii Hook) is a diterpenoid epoxide with induces reactive oxygen species and nephrotubular apoptosis. Cranberry juice is discussed as promoter of kidney stone formation (nephrolithiasis). Abuse of guaifenesin from Roughbark (Guaicum officinale L.) increases stone formation. Aristolochia acids from Aristolochia fangchi Y.C.Wu ex L.D. Chow & S.M. Hwang causes the well-known aristolochic acid nephropathy and carcinogenesis by DNA adduct formation. Carboxyatractyloside from Impila (Callilepsis laureola DC.) inhibits mitochondrial ATP synthesis. Acute allergic interstitial nephritis was diagnosed after intake of Peruvian Cat's claw (Uncaria tomentosa Willd. DC.). Whether or not Willow Bark (Salix alba L.) induces analgesic nephropathwy is a matter of discussion. Other herbal therapies are considered to affect the rennin-angiotensisn-aldosterone (RAA) system Ephedra sinica Stapf with its ingredient ephedrine. Devil'sx Claw (Harpagophytum procumbens DC. Ex Meisn.) and licorice (Glycyrrhiza glabra L.) may inhibit major renal transport processes needed for filtration, secretion, and absorption. Strategies to minimize nephrotoxicity include (1) quality control and standardization of herbal products, (2) research on the molecular modes of action to better understand pathophysiological mechanisms of herbal products as well as (3) clinical trials to demonstrate efficacy and safety.

INTRODUCTION:

Rifampicin is one of the most effective antibiotics for treating tuberculosis, but it has been associated with adverse reactions, such as nephrotoxicity, sometimes resulting in acute renal failure with oligoanuria, and hepatotoxicity. Although deterioration of renal function, determined by acute tubulointerstitial nephritis and/or acute tubular necrosis, typically appears in patients receiving intermittent rifampicin therapy, some authors have also reported cases occurring during continuous rifampicin therapy.

CASE PRESENTATION:

We describe the case of acute renal failure with polyuria occurring in a previously healthy 50-year-old Caucasian man undergoing continuous therapy with rifampicin for culture-confirmed pulmonary tuberculosis. The patient was admitted to the L. Spallanzani National Institute for Infectious Diseases, Rome, Italy, with a 1-month history of coughing, fever and weight loss. After 6 weeks of standard antituberculous treatment, progressive deterioration of his renal function was observed: creatinine levels rose from 38.9mumol/L to 318.2mumol/L and urine volume also progressively increased to reach a state of true polyuria (8 to 10L of urine per day). He was diagnosed with suspected acute rifampicin-induced renal failure. A renal biopsy showed focal segmental glomerulosclerosis associated with acute tubulointerstitial nephritis. Rifampicin was discontinued with excellent results: after 15 days his renal function began to improve and his serum creatinine values returned to normal.

CONCLUSION:

A high index of suspicion for rifampicin-associated acute renal failure should be maintained in patients with pulmonary tuberculosis who develop progressive deterioration of renal function during treatment with rifampicin. Early diagnosis and discontinuation of rifampicin are of fundamental importance for recovering renal function.

We hereby describe a 49-year-old woman with acute renal failure due to tubulointerstitial nephritis and uveitis (TINU) syndrome. This patient presented with vomiting and nausea and was found to have chronic uveitis, elevated creatinine, and interstitial nephritis. The combination of tubulointerstitial nephritis and uveitis emerged the diagnosis of TINU syndrome after a stepwise examination for differential diagnosis. Clinical course and renal function improved quickly on oral steroids but not to normal range. TINU syndrome, although known to some ophthalmologists and nephrologists, is still rather obscure. TINU syndrome should be considered in patients with uveitis in combination with acute renal failure. The prognosis for the renal disorder is excellent, although the uveitis often recurs or remains chronic.

The renal manifestations of patients infected with HIV are diverse. Patients may have podocytopathies ranging from a minimal-change-type lesions to FSGS or collapsing glomerulopathy. Furthermore, such patients produce a variety of autoantibodies without clinical signs of the disease. Antiretroviral drugs also cause renal injury, including crystals and tubular injury, acute interstitial nephritis, or mitochondrial toxicity. In these circumstances, it is essential to perform a renal biopsy for diagnosis and to guide treatment. Here we describe a patient with HIV who presented with AKI and hematuria without concomitant systemic manifestations. Renal biopsy elucidated the cause of acute deterioration of kidney function.

Karyomegalic interstitial nephritis (KIN) is a rare and certainly underdiagnosed nephropathy. It is characterized by a peculiar histological picture of interstitial nephritis associated with the presence of hyperchromatic, abnormally enlarged nuclei of tubular epithelial cells. KIN has an uncertain etiology, but should be suspected in young patients in the second or third decade of life presenting with progressive renal failure, proteinuria and/or hematuria and a history of recurrent respiratory infections. In these cases, the diagnosis should be suspected and confirmed by a renal biopsy. Herein, we report a case of KIN with atypical clinical presentation in a young patient with progressive kidney failure without proteinuria or hematuria or history of recurrent respiratory infections.