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Interstitial nephritis [keywords]
- Changes in the aetiology, clinical presentation and management of acute interstitial nephritis, an increasingly common cause of acute kidney injury. [REVIEW]
- Nephrol Dial Transplant 2014 Oct 16.
Acute interstitial nephritis (AIN) is an important cause of acute kidney injury that has experienced significant epidemiological and clinical changes in the last years. The classical presentation, mostly induced by antibiotics and accompanied by evident hypersensitivity manifestations (skin rash, eosinophilia, fever) has been largely replaced by oligosymptomatic presentations that require a higher index of suspicion and are increasingly recognized in the elderly, having non-steroidal anti-inflammatory agents and proton pump inhibitors as frequent offending drugs. Drug-induced AIN continues to be the commonest type, but it requires a careful differential diagnosis with other entities (tubulointerstitial nephritis with uveitis syndrome, IgG4-related disease, drug reaction with eosinophilia and systemic symptom syndrome, sarcoidosis and other systemic diseases) that can also induce AIN. Cortico-dependant, relapsing AIN is a recently recognized entity that poses an important therapeutic challenge. Although corticosteroids are widely used in drug-induced AIN to speed kidney function recovery and avoid chronic kidney disease, their efficacy has not been tested by randomized controlled trials. New diagnostic tests and biomarkers, as well as prospective therapeutic studies are needed to improve AIN diagnosis and management.
- Granulomatous tubulointerstitial nephritis secondary to omeprazole. [Journal Article]
- BMJ Case Rep 2014.
Drug-induced interstitial nephritis is a common cause of acute kidney injury indicated by elevated serum creatinine. We report a case of omeprazole-induced acute granulomatous interstitial nephritis (GIN). Our patient developed acute GIN secondary to omeprazole ingestion requiring haemodialysis. Treatment with steroids and withdrawal of omperazole was successful allowing the patient to discontinue haemodialysis in 3 months. She remains dialysis free with chronic kidney disease stage IV, reflected by a serum creatine of 191 μmol/L and estimated glomerular filtration rate of 23 mL/min/1.73 m(2) at 5 years on follow-up.
- Characteristics and clinical outcome of nonsteroidal anti-inflammatory drug-induced acute hepato-nephrotoxicity among Chinese patients. [Journal Article]
- World J Gastroenterol 2014 Oct 14; 20(38):13956-65.
To determine the clinicopathological characteristics of nonsteroidal anti-inflammatory drug (NSAID)-induced acute hepato-nephrotoxicity among Chinese patients.We conducted a retrospective chart review of patients using the International Classification of Diseases, Ninth Revision diagnosis code for acute kidney injury (AKI) (584.5 or 584.9) and for acute liver injury (ALI) (570.0 or 573.3) from January 2004 to December 2013. Medical records were reviewed to confirm the diagnosis of AKI and ALI and to quantify NSAID administration.Seven of 59 patients (11.8%) were identified with acute hepato-nephrotoxicity induced by NSAIDs. Five patients (71.4%) received over the recommended NSAIDs dose. Compared with NSAIDs-associated mere AKI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), a high prevalence of alcohol use (71.4%) and positive hepatitis B virus (HBV) markers (85.7%). Compared with NSAIDs-associated mere ALI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), increased extracellular volume depletion (71.4%), and renin-angiotensin-aldosterone system (RAAS) inhibitor combined use (57.1%). Acute interstitial nephritis and acute tubulointerstitial disease were apparent in three out of six (42.9%) kidney biopsy patients, respectively. Acute hepatitis was found in four out of six (66.7%) liver biopsy patients. Overall complete recovery occurred in four patients within a mean of 118.25 ± 55.42 d.The injury typically occurred after an overdose of NSAIDs. The risk factors include age older than 60 years, alcohol use, positive HBV markers, extracellular volume depletion and RAAS inhibitor combined use.
- Renal interstitial mast cell counts differ across classes of proliferative lupus nephritis. [Journal Article]
- Folia Histochem Cytobiol 2014; 52(3):218-24.
Systemic lupus erythematosus frequently involves the kidneys leading to significant morbidity and mortality. It is classified according to glomerular involvement pattern but tubulointerstitial lesions are also important for progression and prognosis, as seen in other kidney glomerular diseases. One of the cell types which participate in this process are mast cells. The aim of the study was to analyze the counts of tryptase-positive and chymase-positive mast cells in lupus nephritis classes II, III and IV. Material consisted of 42 renal biopsies from patients with lupus nephritis; 11 class II, 9 class III and 22 class IV. Chymase- and tryptase-containing cells were stained by immunohistochemistry and counted microscopically. Mean count of chymase-positive mast cells was 9.8/10 high power fields (hpf) for the whole group, 4.66 for class II, 11.89 for class III, and 11.51 for class IV. The mean count of tryptase-positive cells was 18.6/10 hpf for the whole group, 7.65 for class II, 25.57 for class III, and 21.23 for class IV. The differences between lupus nephritis classes were significant both for chymase- and tryptase-positive cells. Tryptase- but not chymase-positive cell counts showed a correlation with the creatinine level (R = 0.35). These results suggest that mast cells are involved to a different degree in the pathogenesis of lupus nephritis depending on the class of the disease.
- The rs1800471 Polymorphism of TGFB1 Gene, Serum TGF-Beta1 Level and Chronic Kidney Disease Progression. [JOURNAL ARTICLE]
- Adv Exp Med Biol 2014 Oct 9.
The aim of the study was to investigate whether rs1800471 polymorphism in TGFB1 gene is associated with the development and progression of non-diabetic chronic kidney disease. Moreover, we examined the serum TGF-beta1 concentration and its association with that polymorphism and progression of the disease. We applied two different methodological approaches. Firstly, a family based study was carried out, comprised of 109 patients with non-diabetic chronic kidney disease and their 218 healthy parents, using the transmission/disequilibrium test. The rs1800471 polymorphism and serum TGF-beta1 level were determined in all subjects. Serum TGF-beta1 concentration was also measured in 40 healthy controls. Secondly, we performed a case-control orientated study to determine whether rs1800471 polymorphism and other factors influence the progression of renal impairment. We found no relationships between rs1800471 polymorphism allele transfer and the incidence or progression of non-diabetic chronic kidney disease. We found, however, that the serum TGF-beta1 was significantly higher in patients than in controls. In conclusion, rs1800471 polymorphism in TGFB1 gene does not have an impact on the development and progression of non-diabetic chronic kidney disease caused by primary glomerulopathy and chronic interstitial nephritis. The increased serum TGF-beta1 concentration in such patients suggests its role in the pathomechanism of the disease. Circulating TGF-beta1 level is determined in a multifactorial way, not by rs1800471 polymorphism in TGFB1 gene.
- [Pharmacogenetic aspects of candesartan application for the treatment of arterial hypertension in patients with chronic pyelonephritis]. [English Abstract, Journal Article]
- Lik Sprava 2014 Mar-Apr; (3-4):119-25.
Now necessity of the strict control arterial pressure (AP) is conventional at chronic diseases of kidneys. Inhibitors of receptors AT1R (BAR) are recognized all over the world as preparations of the first of some for treatment of renoparenchimal hypertensia. The purpose research--to study of clinical effect of Candesartan at patients with renoparenchimal hypertensia depending on a genotype. Survey 50 patients with inspected patients with renoparenchimal hypertensia on a background of chronic pyelonephritis, polymorphism of gene of angiotensin 11 of the first type is certain. Patients appointed Kandesartan in doses of 8-32 (Mg), observed in current of 12 months. By results of research the genotype AA is revealed at 46%, AC at 48%, CC at 6% of patients. Allel A it is revealed in a genotype of 94%, allel C - 54% of patients of renoparenchimal hypertensia. A target level the AP will reach at 94.,3% patients. Kandesartan has shown high clinical effect at all variants of polymorphism of gene AT1R.
- Lupus erythematosus tumidus: a unique disease entity. [Journal Article]
- Hawaii J Med Public Health 2014 Sep; 73(9 Suppl 1):18-21.
Lupus erythematosus tumidus (LET) is a photosensitive skin disease characterized by succulent, edematous, and non-scarring plaques. Histologic features include perivascular and periadnexal lymphocytic infiltration and interstitial mucin deposition. Despite being first described in 1909, there are few case reports in the current literature describing this disease and even fewer that discuss treatment. We describe a case of a 22-year-old woman with systemic lupus erythematosus (SLE) and secondary class V lupus nephritis. She was referred to Dermatology for an intermittent pruritic facial eruption that was clinically and histologically consistent with LET. There is much controversy in literature as to whether or not LET is a unique variant of cutaneous lupus erythematosus. Interestingly, the mainstay of treatment for LET, in the limited case reports and series that exist, is with antimalarial drugs, which our patient had already been taking for SLE. This case exemplifies the need for complete disease characterization, evidence-based treatment, and a multidisciplinary approach.
- Autoimmune pancreatitis with colonic stenosis: an unusual complication and atypical pancreatographic finding. [JOURNAL ARTICLE]
- BMC Gastroenterol 2014 Oct 3; 14(1):173.
Type 1 autoimmune pancreatitis (AIP) often accompanies various systematic disorders such as sclerosing cholangitis, sialoadenitis, retroperitoneal fibrosis, interstitial pneumonitis and nephritis. Although rarely reported in acute pancreatitis, colonic stenosis is an uncommon complication in cases with AIP.A 69-year-old Japanese man complained of abdominal pain and continuous diarrhea, resistant to intake of antimuscarinic and probiotic agents. A colonoscopy demonstrated a stenosis at the splenic flexure. Computed tomography revealed a focal enlargement of the pancreatic tail with a capsule-like rim, contacting with the descending colon. Endoscopic retrograde pancreatography (ERP) was unable to visualize the main pancreatic duct (MPD) at the pancreatic tail, despite a full contrast injection. A high serum IgG4 level (1060 mg/dL) and exclusion of pancreatic cancer by endoscopic ultrasound guided-fine needle aspiration suggested AIP, but did not fulfill the diagnostic criteria, and steroid therapy was initiated. One month after starting steroid intake, pancreatic swelling was minimized and the MPD was visualized by ERP, fulfilling the international consensus diagnostic criteria (ICDC) of AIP. Colonic stenosis was relieved and the patient's symptoms disappeared.The present case is the first report of AIP developing colonic stenosis by the inflammatory infiltration. In this case, steroid therapy was effective for the diagnosis and treatment of pancreatic mass involving the descending colon.
- Images in clinical medicine. Chronic obstructive pyelonephritis. [Case Reports, Journal Article]
- N Engl J Med 2014 Oct 2; 371(14):1332.