Effects of aristolochic acid I and/or hypokalemia on tubular damage in C57BL/6 rat with aristolochic acid nephropathy
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Background/Aims This study was designed to investigate the roles of aristolochic acid I (AA-I) and hypokalemia in acute aristolochic acid nephropathy (AAN). Methods After an adaptation period (1 week), a total of 40 C57BL/6 mice (male, 8 weeks old) were divided into four groups: I (control group), II (low potassium [K] diet), III (normal K diet with administration of AA-I [10 mg/kg weight]), and IV (low K diet with AA-I). After collecting 24 hours of urine at 2 weeks, the mice were sacrificed, and their blood and kidneys were obtained to perform immunochemical staining and/or Western blot analysis. Results Proteinuria, glycosuria, and increased fractional excretion of sodium and K were prominent in groups III and IV (p < 0.05). Diffuse swelling and poor staining of collecting duct epithelial cells were evident in the medullas of group II. Typical lesions of toxic acute tubular injury were prominent in the cortices of groups III and IV. Α-Smooth muscle actin (α-SMA) was higher in the cortices of the mice in groups III and IV versus group II (p < 0.05), and higher in the medullas of group IV than groups I and III (p < 0.05). E-cadherin was higher in the cortices of groups III and IV compared to group I (p < 0.05). The F4/80 value was higher in the cortices and medullas of groups II, III, and IV compared to group I (p < 0.05), particularly in the case of group II. Conclusions AA-I can induce acquired Fanconi syndrome in the acute stage of AAN. Macrophages appear to play a key role in the pathogenesis of AAN and hypokalemic nephropathy. It remains uncertain whether hypokalemia plays any role in AAN and hypokalemia.Keywords:
Aristolochic Acid
Glycosuria
Objective:To study the clinicopathological difference between the aristolochic acid nephropathy and IgA nephropathy with chronic renal failure.Methods:11 patients of aristolochic acid nephropathy with chronic renal failure in our division were reviewed and their clinical,laboratory and pathologic manifestations were analyzed as compared to IgA nephropathy patients by one-to-one matched design (paired).Results:Age, sex, and serum creatinine lever were not statistically different between the two groups. The group of aristolochic acid nephropathy showed lower incidence of hematuria than IgA nephropathy group (P0.05).The lower lever of serum hemoglobin,proteinuria and kidney size were observed in the group of aristolochic acid nephropathy than IgA nephropathy group (P0.05) while serum creatinine lever were not statistically different. Heavier interstitial fibrosis and fewer inflammatory cells in the interstitium were also shown in the group of aristolochic acid nephropathy.Conclusion:Aristolochic acid nephropathy with chronic renal failure progresses with no obvious clinic manifestations as compared to IgA nephropathy. Serious tubular atrophy and interstitial fibrosis are main pathologic characteristics. It is important to diagnose and treat aristolochic acid nephropathy early.
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The condition existing in the patient whom we are about to describe is usually referred to in medical literature as renal glycosuria. In addition to this term, the literature contains several designations which have reference to the same symptom-complex. John1objects to the term renal glycosuria because "all glycosuria is renal in origin, depending upon the renal threshold as well as the glycemic level"; he suggests the term nondiabetic glycosuria. Umber and Rosenberg2speak of renal diabetes or glycosuria innocens. Cyclic renal glycosuria or cyclic glycosuria is a subgroup of renal glycosuria described by Jonas3and Faber.4Benign glycosuria is a group term including the glycosurias of nondiabetic origin. The diagnosis of renal glycosuria may be made in cases in which there exists a chronic, nonprogressive, apparently harmless glycosuria without the symptoms of diabetes and without hyperglycemia in the fasting or postabsorptive states. The renal threshold
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In defining renal glycosuria, Strouse1gives four points of differentiation from diabetes mellitus: (1) glycosuria without hyperglycemia; (2) glycosuria almost entirely independent of carbohydrate intake; (3) absence of diabetic symptoms, and (4) no subsequent development of diabetes mellitus. Paullin2has added a fifth characteristic in this condition, that sugar shall be constantly present in the urine. That renal glycosuria shall not later become diabetes mellitus necessitates a prolonged observation of such patients, and this is the reason for reporting a case in which glycosuria was discovered eighteen years ago, the patient having been employed in a hospital for the sake of supervision for the last nine years. Bailey3has reported a case in which glycosuria has been known for ten years, and says, "The patient's history points strongly to this being a congenital condition." Strouse has observed a case for eight years, Garrod4and Bonninger5
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There have been numerous domestic and international reports of nephrotoxicity associated with botanical products found to contain aristolochic acid. Many investigations disclosed cases of nephropathy and end-stage renal diseases associated with ingestion of products containing aristolochic acid. Of further concern is carcinogenic potential of aristolochic acid. Aristolochic acid, when tested for carcinogenicity by oral administration in mice and rats,induced chronically toxicity,and led to local and systemic tumors. Furthermore,patients taking aristolochic acid may be at increased risk of developing malignancies. The toxic effects of aristolochic acid in animals have been inferred from effects seen in patients suffering from kidney nephropathy as a result of consuming herbal mixtures containing aristolochic acid. Concerns about botanical-containing products known or suspected of containing aristolochic acid will bring to our attention important safety information relative to nephrotoxicity associated with aristolochic acid and rationality to utilize traditional Chinese medicine.
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Nephrotoxicity
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Covering: 1960 to 2013
Aristolochic Acid
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Aristolochia
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Aristolochic Acid
Aristolochia
Aristolochiaceae
Nephrotoxicity
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Aristolochic acid nephropathy is a chronic, fibrosing, interstitial nephritis caused by aristolochic acid (AA), which is a component of the plants of Aristolochiacae family. It was first reported in 1993, in Belgium as a Chinese herb nephropathy, in patients who received a slimming regimen containing AA. The term aristolochic acid nephropathy also includes Balcan endemic nephropathy and other endemic tubulointerstitial fibrosis. Moreover, AA is a human carcinogen which induces urothelial cancer. The AA-containing herbs are banned in many countries and FDA published the warnings concerning the safety of AA-containing botanical remedies in 2000. Regarding the increasing interest in herbal medicines, uncontrolled access to botanical remedies and replacement of one herb by another AA-containing compounds makes thousands of people all around the world at risk of this grave disease.
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In this article, the proposal to rename “Chinese herbs nephropathy” was reviewed. Prolonged use of Chinese herbs that contain aristolochic acid may induce tubulo-interstitial disorders. In our opinion, the “Chinese herbs nephropathy” nomenclature is equivocal, and should be changed to “aristolochic-acid nephropathy”. Professor Vanherweghem, who is the first author to write about this disease, also used the name “Aristolochia nephropathy.”
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