1/15. Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid.mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induction of tubulointerstitial damage. Excess iodine ingestion is known to produce toxicity and possible death, but acute renal failure is rare. There is evidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. iodine has not been documented to produce red cell hemolysis and hemoglobinuria. We present a unique case of acute renal failure from hemoglobinuric and acute interstitial nephritis secondary to suicidal ingestion of potassium iodide solution and also ingestion of a few mefenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfunction from alteration of renal perfusion by selective COX-1 inhibition of prostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hemodialysis and supportive therapy.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/15. Interstitial nephritis associated with glomerulonephritis in a patient with Hashimoto's disease and idiopathic portal hypertension.A middle-aged women with hypothyroidism, idiopathic portal hypertension and nephrotic syndrome is presented. This unusual clinical appearance could not be explained as SLE by serological examinations. Pathohistological examinations showed "Banti's liver", Hashimoto's thyroiditis and diffuse proliferative glomerulonephritis with severe tubulo-interstitial nephritis. Immunohistochemical studies revealed IgA deposits in glomeruli. Electron microscopic study disclosed peculiar lucent areas of rarefaction with osmiophilic particles in tubular basement membranes. This tubulointerstitial nephritis was considered to be related to the immunological mechanism involving thyroid gland, liver and kidney disorders. This case thus had a clinically rare combination of these three.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
3/15. Proximal tubular dysfunction in primary sjogren's syndrome: a clinicopathological study of 2 cases.Tubulointerstitial nephritis is the most common renal complication in primary sjogren's syndrome (SS). It is usually associated with symptoms of distal tubular dysfunction, type I (distal) renal tubular acidosis (RTA) and nephrogenic diabetes insipidus. Proximal tubular abnormalities are considered to be less frequent, and Fanconi's syndrome has been only exceptionally reported in patients with SS. We describe 2 patients with primary SS, characterized by xerostomia, dry eyes, extensive lymphocytic infiltrate on salivary gland biopsy, positive tests for anti-SSA/SSB antibodies and/or antinuclear antibodies, who presented in renal failure with proteinuria, microscopic hematuria and type I RTA. Further studies revealed proximal tubular dysfunction, including renal glucosuria, generalized aminoaciduria, phosphaturia, uricosuria, together with proximal (type II) RTA in 1 case. Neither of these patients had Bence Jones proteinuria or monoclonal gammopathy. kidney biopsy showed focal proximal tubulitis, associated with proximal tubular cell atrophy and dedifferentiation, and diffuse interstitial nephritis with fibrosis. No significant glomerular or peritubular deposits of immunoglobulin light or heavy chain were observed. These findings demonstrate that diffuse, distal and proximal, tubular dysfunction may occur in patients with SS and interstitial nephritis. Lymphocytic infiltration of proximal tubular cells is probably involved in the pathogenesis of Fanconi's syndrome in SS. However, the mechanisms involved in the alteration of sodium-dependent apical transports remain to be elucidated.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
4/15. A case of Mikulicz's disease complicated with interstitial nephritis successfully treated by high-dose corticosteroid.A 40-year-old woman who had bilateral swelling in the eyelids and submandibular region was admitted. Clinical findings suggested she had primary sjogren's syndrome. Laboratory data showed glucosuria, positive CRP (0.50 mg/dl), liver dysfunction (AST 53 U/l, ALT 101 U/l, gamma-GTP 241 U/l, ALP 914 U/l, LAP 496 U/l), hyperglycemia, hypergammaglobulinemia (IgG 3450 mg/dl, IgA 91 mg/dl, IgM 80 mg/dl), hypocomplementemia (C3 73 mg/dl, C4 2 mg/dl, CH50 < 19.0 U/ml), renal tubular dysfunction (urine N-acetyl-beta-D: -glucosaminidase 8.6 U/l, urine (beta2)-microglobulin 83 microg/l), and urinary concentration defect. ammonium chloride loading test was normal. gallium-67 scintigram indicated abnormal uptake in bilateral lacrimal glands, submandibular glands, and kidneys. A diagnosis of Mikulicz's disease and interstitial nephritis was made, since biopsy specimens of her lacrimal gland and minor salivary gland showed diffuse infiltration of lymphocytes. Renal biopsy specimens also showed severe interstitial infiltration of lymphocytes. Symptoms and laboratory data normalized in response to methylprednisolone pulse therapy and prednisolone 60 mg/day. This case of Mikulicz's disease complicated with interstitial nephritis was successfully treated by high-dose corticosteroid.- - - - - - - - - - ranking = 4keywords = gland (Clic here for more details about this article) |
5/15. Tubulointerstitial nephritis and uveitis syndrome associated with hyperthyroidism.We report a 17-year-old male patient with tubulointerstitial nephritis and uveitis (TINU) associated with hyperthyroidism. He presented with a 2-month history of fatigue, loss of appetite, low-grade fever, and a 12-kg weight loss when he was admitted to our hospital. He had iritis, which was complicated by fibrin in the anterior chamber, diagnosed by slit-lamp examination. On laboratory examinations, deteriorated renal function (blood urea nitrogen level was 25.9 mg/dl and creatinine level was 2.82 mg/dl) and elevated urinary levels of N-acetyl-beta-D-glucosaminidase (33.1 U/l) and beta2-microglobulin (78,600 microg/l) were observed. serum thyroid-stimulating hormone (TSH) was undetectable, at less than 0.01 microIU/ml, and free triiodothyronine and free thyroxine were elevated, up to 5.23 pg/ml and 2.85 ng/dl, respectively. The titers of antithyroglobulin and antithyroid microsomal and TSH-receptor antibodies were not elevated. Abdominal and thyroidal ultrasonography showed evident bilateral enlargement of the kidneys and diffuse enlargement of the thyroid gland. iodine-123 scintigraphy showed low uptake in the thyroid gland. The biopsied renal specimen showed mild edema and severe diffuse infiltration of mononuclear cells and few eosinophils in the interstitium, without any glomerular or vascular abnormalities. Based on the clinical features and pathological findings, a diagnosis of TINU syndrome with associated hyperthyroidism was made. Treatment was started with 30 mg/day of prednisolone. The iritis disappeared, and the patient's clinical status improved remarkably. This case suggests the possibility of thyroid dysfunction in some patients with TINU syndrome, and we believe thyroid function should be measured in all TINU patients. Moreover, histopathological diagnosis of the thyroid glands before treatment is necessary for TINU patients with thyroid dysfunction.- - - - - - - - - - ranking = 3keywords = gland (Clic here for more details about this article) |
6/15. Characterization of immune cells in kidneys from patients with sjogren's syndrome.The association of interstitial nephritis, the most common renal lesion in sjogren's syndrome, to the other manifestations of the disease is unclear. To begin to address this issue, the infiltrating cells in frozen kidney tissues from two patients with interstitial nephritis secondary to sjogren's syndrome were characterized by indirect immunofluorescence. T cells predominated, the majority of which were helper/inducer cells (OKT4 ). Both kidneys contained nodules of B cells. The increased proportion of OKT4 T cells in salivary gland and in interstitial renal lesions of sjogren's syndrome contrasts with some other forms of interstitial renal disease and suggests that the renal and salivary gland lesions have a similar pathogenesis.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |
7/15. T lymphocyte subsets of the infiltrating cells in the salivary gland and kidney of a patient with sjogren's syndrome associated with interstitial nephritis.lymphocyte subsets in the salivary gland and kidney were examined in a 38 years-old female patient with sjogren's syndrome associated with interstitial nephritis by PAP immunoperoxidase method using monoclonal antibodies. Predominant cells of the infiltrating cells in both tissues were T lymphocytes and most of them were Ia , OKT4 cells (activated helper/inducer T lymphocytes). A small number of T lymphocytes were OKT8 (suppressor/cytotoxic T lymphocytes). Moreover, we found the OKT8 cells invading the salivary duct epithelial cells. There was no difference in the proportion of lymphocyte subsets of the infiltrating cells between the salivary gland and kidney. A similar pathologic mechanism of tissue damage, therefore, was suggested in both tissues.- - - - - - - - - - ranking = 6keywords = gland (Clic here for more details about this article) |
8/15. Nephrotoxicity of nonsteroidal anti-inflammatory drugs.Most nonsteroidal anti-inflammatory drugs can cause a variety of adverse renal effects when used in therapeutic doses. These effects range from elevation of BUN and creatinine to renal failure. Prostaglandin inhibition and T-lymphocyte disorder are believed to be the pathogenic factors. The effects are generally reversible with discontinuance of the drug, but some patients may require supportive management with hemodialysis and therapy with immunosuppressive agents.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
9/15. piroxicam-induced renal disease.Two cases of nephrotoxicity associated with piroxicam therapy are reported. In the first case, severe reversible azotemia with hyperkalemia resolved after discontinuation of the medication. In the second case, biopsy-proved acute interstitial nephritis with immune complex glomerulonephritis and hepatitis improved after steroid therapy. The mechanism for such toxicity may be altered hemodynamics, cellular immunity, or humoral immunity related to prostaglandin inhibition.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
10/15. indomethacin-induced hyperkalemia in three patients with gouty arthritis.We describe three patients in whom severe, life-threatening hyperkalemia and renal insufficiency developed after treatment of acute gouty arthritis with indomethacin. This complication may result from an inhibition of prostaglandin synthesis and consequent hyporeninemic hypoaidosteronism. Careful attention to renal function and potassium balance in patients receiving indomethacin or other nonsteroidal anti-inflammatory agents, particularly in those patients with diabetes mellitus or preexisting renal disease, will help prevent this potentially serious complication.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
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