Pathophysiology and Clinical Aspects of Drug-Induced Tubular Necrosis in Man

2015 ◽  
pp. 145-158 ◽  
Author(s):  
D. Kleinknecht ◽  
P. Landais ◽  
B. Goldfarb
Keyword(s):  
Clinical Aspects ◽  
Drug Induced ◽  
Tubular Necrosis

All That Glitters Yellow Is Not Gold: Presentation and Pathophysiology of Bile Cast Nephropathy

2017 ◽  
Vol 25 (7) ◽  
pp. 652-658 ◽  
Author(s):  
Mitchell Pitlick ◽  
Prerna Rastogi
Keyword(s):  
Liver Disease ◽  
Kidney Biopsy ◽  
Kidney Injury ◽  
Renal Tubules ◽  
Drug Induced ◽  
Underlying Liver Disease ◽  
Drug Induced Liver Injury ◽  
Tubular Necrosis ◽  
Cast Nephropathy ◽  
Severe Hyperbilirubinemia

Background. Acute kidney injury (AKI) often manifests in patients with liver disease because of a prerenal cause and presents as acute tubular necrosis or hepatorenal syndrome. Distinguishing between these entities is important for prognosis and treatment. Some patients may develop AKI related to their underlying liver disease: for example, membranoproliferative glomerulonephritis or IgA nephropathy. Bile cast nephropathy is an often ignored differential diagnosis of AKI in the setting of obstructive jaundice. It is characterized by the presence of bile casts in renal tubules, which can possibly cause tubular injury through obstructive and direct toxic effects. Thus, AKI in patients with liver disease may have a structural component in addition to a functional one. Methods. In this study, we describe 2 patients with severe hyperbilirubinemia who developed AKI and underwent a kidney biopsy that revealed bile casts in tubular lumens, consistent with bile cast nephropathy. Results. One patient was treated aggressively for alcoholic hepatitis and required hemodialysis for AKI. The second patient was treated conservatively for drug-induced liver injury and did not require dialysis. Both patients saw a reduction in their bilirubin and creatinine toward baseline. Conclusion. Bile cast nephropathy is an important pathological entity that may account for the renal dysfunction in some patients with liver disease. It requires kidney biopsy for diagnosis and may often be overlooked given the scarcity of kidney biopsy in this particular clinical setting. The etiology is multifactorial, and it is often difficult to predict without the aid of a renal biopsy.

Drug-Induced Aplastic Anemia: Pathogenesis and Clinical Aspects

1990 ◽  
Vol 12 (4) ◽  
pp. 402-410 ◽  
Author(s):  
David Malkin ◽  
Gideon Koren ◽  
E. Fred Saunders
Keyword(s):  
Aplastic Anemia ◽  
Clinical Aspects ◽  
Drug Induced

scholarly journals Drug-induced acute tubular necrosis

2020 ◽  
pp. 49-62
Author(s):  
O.D. Ostroumova ◽  
◽  
M.V. Klepikova ◽  
K.K. Dzamikhov ◽  
V.A. De ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Tubular Necrosis ◽  
Kidney Damage ◽  
Drug Induced ◽  
Main Method ◽  
Tubular Necrosis ◽  
Risk Of Mortality ◽  
History Of ◽  
Nephrotoxic Drugs ◽  
Management Schemes

Nowadays, there is an increasing necessity to use a lot of medical products (MP) in one patient. This can lead to potential nephrotoxic adverse reactions (ADRs) among drugs. One of drug-induced kidney damage manifestations is acute tubular necrosis (ATN), which causes the development of severe complications associated with the use of hemodialysis and a high risk of mortality. The purpose of this review is to analyze literature data concerning groups of drugs and individual drugs, the intake of which is associated with the development of drug-induced ATN, risk factors, prevention and treatment methods. Among drug-induced ATN development risk factors are both general, associated with the development of drug-induced acute kidney damage (for example, age, history of chronic kidney disease, etc.), and specific ones, typical for certain groups of drugs. Most often, drug-induced ATN develops while taking antibacterial, antiviral and anticancer drugs. The main method of treatment for drug-induced ATN is abolition of nephrotoxic drugs, but if it is impossible, then there are certain patient management schemes. To prevent and to diagnose drug-induced ATN at early stages, that is the key for favorable prognosis, it is necessary to aware of doctors of different specialties about such pharmacotherapy complications.

scholarly journals Serology of Lupus Erythematosus: Correlation between Immunopathological Features and Clinical Aspects

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Emanuele Cozzani ◽  
Massimo Drosera ◽  
Giulia Gasparini ◽  
Aurora Parodi
Keyword(s):  
Lupus Erythematosus ◽  
Clinical Manifestations ◽  
Clinical Aspects ◽  
Great Effort ◽  
Neuropsychiatric Lupus ◽  
Glomerular Injury ◽  
Drug Induced ◽  
Neonatal Lupus Erythematosus ◽  
Heterogenous Group ◽  
Ribosomal P

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the aberrant production of a broad and heterogenous group of autoantibodies. Even though the presence of autoantibodies in SLE has been known, for more than 60 years, still nowadays a great effort is being made to understand the pathogenetic, diagnostic, and prognostic meaning of such autoantibodies. Antibodies to ds-DNA are useful for the diagnosis of SLE, to monitor the disease activity, and correlate with renal and central nervous involvements. Anti-Sm antibodies are highly specific for SLE. Anti-nucleosome antibodies are an excellent marker for SLE and good predictors of flares in quiescent lupus. Anti-histone antibodies characterize drug-induced lupus, while anti-SSA/Ro and anti-SSB/La antibodies are associated with neonatal lupus erythematosus and photosensitivity. Anti-ribosomal P antibodies play a role in neuropsychiatric lupus, but their association with clinical manifestations is still unclear. Anti-phospholipid antibodies are associated with the anti-phospholipid syndrome, cerebral vascular disease, and neuropsychiatric lupus. Anti-C1q antibodies amplify glomerular injury, and the elevation of their titers may predict renal flares. Anti-RNP antibodies are a marker of Sharp’s syndrome but can be found in SLE as well. Anti-PCNA antibodies are present in 5–10% of SLE patients especially those with arthritis and hypocomplementemia.

Antiviral Drugs and Acute Kidney Injury (AKI)

2019 ◽  
Vol 19 (4) ◽  
pp. 375-382 ◽  
Author(s):  
Wattana Leowattana
Keyword(s):  
Acute Kidney Injury ◽  
Antiviral Drug ◽  
Kidney Injury ◽  
Rapid Onset ◽  
Antiviral Drugs ◽  
Drug Induced ◽  
Common Cause ◽  
True Prevalence ◽  
Tubular Necrosis ◽  
Crystal Nephropathy

The introduction of more efficient antiviral drugs are common cause drug-induced acute kidney injury (AKI). The true prevalence of antiviral drugs induced nephrotoxicity is hardly determined. It causes AKI by many mechanisms including acute tubular necrosis (ATN), allergic interstitial nephritis (AIN), and crystal nephropathy. ATN has been described with a few kinds of antiviral drugs such as cidofovir, adefovir and tenofovir with unique effects on transporter defects, apoptosis, and mitochondrial injury. AIN from atazanavir is a rapid onset of AKI and usually nonoliguric but dialytic therapy are needed because of severity. Additionally, crystal nephropathy from acyclovir, indinavir, and foscarnet can cause AKI due to intratubular obstruction. In this article, the mechanisms of antiviral drug-induced AKI were reviewed and strategies for preventing AKI were mentioned.

Acute Renal Failure Amongst Children in a Tropical Environment

1987 ◽  
Vol 10 (2) ◽  
pp. 97-101 ◽  
Author(s):  
K.S. Chugh ◽  
A. Narang ◽  
L. Kumar ◽  
V. Sakhuja ◽  
V. Narayanan Unni ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Rural Areas ◽  
Acute Interstitial Nephritis ◽  
Acute Glomerulonephritis ◽  
Drug Induced ◽  
Tubular Necrosis ◽  
Renal Histology ◽  
Endocapillary Proliferative Glomerulonephritis ◽  
Glucose 6 Phosphate Dehydrogenase

The pathogenetic factors leading to acute renal failure (ARF) in 223 children between the ages of 20 days and 14 years were studied. Diarrhoeal diseases were responsible for ARF in 49.8%, acute glomerulonephritis in 34.1%, drug induced intravascular hemolysis in glucose -6-phosphate dehydrogenase deficiency in 4.5%, snake bite in 4%, hemolytic uremic syndrome in 2.2%, and miscellaneous causes in 5.4%. Dialysis was instituted in 178 children and the others were treated conservatively. Renal histology in 39 out of 76 children who presented with an acute nephritic illness revealed acute endocapillary proliferative glomerulonephritis in 27 and crescentic glomerulonephritis in 12. The histology in 79 out of 147 remaining patients showed acute tubular necrosis in 64, acute cortical necrosis in 13, and acute interstitial nephritis in 2. Overall mortality was 27.4%. This high incidence of ARF due to infective diarrhoeas and dysentery reflects poor socio-economic and hygienic conditions, inadequate facilities in rural areas, delays in seeking medical advice, and lack of knowledge about fluid and electrolyte therapy amongst the staff.

scholarly journals Isoniazid - induced chronic cutaneous Lupus erythematosus

2016 ◽  
Vol 13 (1) ◽  
pp. 52-56
Author(s):  
A Chiriac ◽  
P Brzezinski ◽  
A E Chiriac ◽  
L Foia ◽  
D Mihaila ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Histopathological Examination ◽  
Cutaneous Lupus Erythematosus ◽  
Clinical Aspects ◽  
Direct Immunofluorescence ◽  
Drug Induced ◽  
Systemic Involvement ◽  
Antituberculosis Therapy ◽  
The Face ◽  
Cutaneous Lupus

A 23-year-old man developed drug-induced chronic cutaneous lupus erythematosus 8 months after isoniazid (INH) therapy for pulmonary tuberculosis. Diagnosis was based on clinical aspects (discoid lesions on the face, erythema, photosensitivity, hyperpigmentation), histopathological examination, along with direct immunofluorescence examination (DIF), the absence of systemic involvement and the routine laboratory parameters, which registered all within normal range. Hydroxychloroquine therapy associated to photo protection and emollients determined the clear up of the facial eruption within six months. Transient residual hyperpigmentation could be noticed 2 months after discontinuation of the treatment. This case illustrates a rare form of drug-induced chronic cutaneous lupus erythematosus developed 2 months after withdrawal of antituberculosis therapy, with excellent results with hydroxychloroquine.NJDVL Vol. 13, No. 1, 2015 Page: 52-56

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