Drug-Induced Renal Stones: Incidence, Clinical Expression and Stone Analysis

2015 ◽  
pp. 25-29 ◽  
Author(s):  
A. Rapado ◽  
M. L. Traba ◽  
C. Caycho ◽  
L. Cifuentes-Delatte
Keyword(s):  
Renal Stones ◽  
Stone Analysis ◽  
Clinical Expression ◽  
Drug Induced

Drug-Induced Renal Stones

2010 ◽  
pp. 225-237 ◽  
Author(s):  
Michel Daudon ◽  
Paul Jungers
Keyword(s):  
Renal Stones ◽  
Drug Induced

scholarly journals Impact of Residual Fragments following Endourological Treatments in Renal Stones

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Cenk Acar ◽  
Cag Cal
Keyword(s):  
Treatment Success ◽  
Renal Stones ◽  
Renal Calculi ◽  
Stone Analysis ◽  
Flexible Ureterorenoscopy ◽  
Active Monitoring ◽  
Annual Basis ◽  
Study Results ◽  
Interventional Therapies ◽  
Residual Fragments

Today, shock wave lithotripsy (SWL), percutaneous nephrolithotomy (PCNL), and flexible ureterorenoscopy (URS) are the most widely used modalities for the management of renal stones. In earlier series, treatment success of renal calculi assessed with KUB radiography, ultrasound, or intravenous pyelography which are less sensitive than CT that leads to be diversity of study results in reporting outcome. Residual fragments (RFs) after interventional therapies may cause pain, infection, or obstruction. The size and location of RFs following SWL and PCNL are the major predictors for clinical significant symptoms and stone events requiring intervention. There is no consensus regarding schedule for followup of SWL, PCNL, and flexible URS. Active monitoring can be recommended when the stones become symptomatic, increase in size, or need intervention. RFs <4 mm after SWL and <2 mm after PCNL and flexible URS could be actively monitored on an annual basis with CT. Early repeat SWL and second-look endoscopy are recommended after primary SWL and PCNL, respectively. There is insufficient data for flexible URS, but RFs can be easily treated with repeat URS. Finally, medical therapy should be tailored based on the stone analysis and metabolic workup that may be helpful to prevent regrowth of the RFs.

Nephrolithiasis

2016 ◽  
Author(s):  
Peregrine Dalziel ◽  
Nicholas Schirmer
Keyword(s):  
Prediction Rule ◽  
Clinical Prediction Rule ◽  
Renal Stones ◽  
Renal Calculi ◽  
Renal Calculus ◽  
Ultrasound Images ◽  
Drug Induced ◽  
Size Category ◽  
Test Characteristics ◽  
Twinkling Artifact

The term nephrolithiasis, often used synonymously with urolithiasis, refers to the formation of solid concretions consisting of both protein and crystalline materials in the lumen of the urinary tract. These calculi, or “stones,” become symptomatic when they cause acute obstruction, and as such, there are an unknown but probably large number of individuals with nephrolithiasis who are subclinical, without signs or symptoms. This review covers the pathophysiology, stabilization and assessment, diagnosis, and treatment of nephrolithiasis. Figures show ultrasound images of a stone with shadowing, a stone with a twinkling artifact, hydronephrosis, and a stone with shadowing at the ureterovesicular junction and a computed tomographic (CT) image showing a renal calculus at the ureterovesicular junction. Tables list drug-induced renal calculi, the proportion of stones spontaneously passing depending on size category as identified on CT, diagnostic test characteristics for renal colic diagnosis, the clinical prediction rule for the risk of renal stones, an example of the theoretical probability of stone disease using Moore and colleagues’ risk stratification, pooled test characteristics, bayesian analysis, and important pathology diagnosed on CT scan in the investigation of flank pain in four studies.   Key words: kidney stone, nephrolithiasis, renal calculus, renal stone, urolithiasis This review contains 5 highly rendered figures, 6 tables, and 75 references.

Measuring renal function in old age

2008 ◽  
Vol 18 (4) ◽  
pp. 257-267
Author(s):  
Sanghamitra Chakrabarti ◽  
Indrajit Chattopadhyay
Keyword(s):  
Renal Function ◽  
Old Age ◽  
Renal Stones ◽  
Renal Tubules ◽  
Older Individuals ◽  
Vascular Changes ◽  
Drug Induced ◽  
Functional Changes ◽  
Age Related ◽  
Tract Infections

Accurate assessment of renal function is vital, especially in older individuals, as this is the population in which the greatest burden of chronic kidney disease (CKD) occurs. With ageing, the kidneys undergo a multitude of structural and functional changes. The age-related changes in the kidneys may be further complicated by concurrent pre-renal, renal and post-renal factors common in old age, such as hypertensive glomerulosclerosis, diabetic nephropathy, congestive cardiac failure, renovascular atheroma, urinary outflow obstruction, urinary tract infections, renal stones and drug-induced nephrotoxicity. Structurally, there is a progressive loss of predominantly cortical renal mass, a decrease in the number of glomeruli, an increase in the proportion of sclerotic glomeruli, tubulo-interstitial changes resulting in fibrosis and atrophy, arteriosclerotic vascular changes and a reduction in renal blood flow. Excretory and reabsorptive capacities of the renal tubules may also decline with ageing. Functionally, although there may be a decline in the glomerular filtration rate (GFR) resulting primarily from a reduction in the number of functioning nephrons, this decline may not be universal. Up to a third of elderly people may not demonstrate a decline in GFR with ageing, whilst in some individuals GFR may actually increase with age.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

Effect of piperacillin on morphology and viability of gram-negative bacteria

1984 ◽  
Vol 42 ◽  
pp. 218-219
Author(s):  
R. H. Liss
Keyword(s):  
Inhibitory Concentration ◽  
Cytoplasmic Membrane ◽  
Drug Binding ◽  
Gram Negative Bacteria ◽  
Bacterial Cells ◽  
Drug Induced ◽  
Penicillin Binding Proteins ◽  
Lactam Antibiotic ◽  
Drug Free ◽  
Tube Dilution

Piperacillip (PIP) is b-[D(-)-α-(4-ethy1-2,3-dioxo-l-piperzinylcar-bonylamino)-α-phenylacetamido]-penicillanate. The broad spectrum semisynthetic β-lactam antibiotic is believed to effect bactericidal activity through its affinity for penicillin-binding proteins (PBPs), enzymes on the bacterial cytoplasmic membrane that control elongation and septation during cell growth and division. The purpose of this study was to correlate penetration and binding of 14C-PIP in bacterial cells with drug-induced lethal changes assessed by microscopic, microbiologic and biochemical methods.The bacteria used were clinical isolates of Escherichia coli and Pseudomonas aeruginosa (Figure 1). Sensitivity to the drug was determined by serial tube dilution in Trypticase Soy Broth (BBL) at an inoculum of 104 organisms/ml; the minimum inhibitory concentration of piperacillin for both bacteria was 1 μg/ml. To assess drug binding to PBPs, the bacteria were incubated with 14C-PIP (5 μg/0.09 μCi/ml); controls, in drug-free medium.

Drug Induced Changes in Cell Organelles

1968 ◽  
Vol 26 ◽  
pp. 110-111
Author(s):  
Sarah A. Luse
Keyword(s):  
Clinical Medicine ◽  
Cell Organelles ◽  
Riboflavin Deficiency ◽  
Drug Induced ◽  
New Era ◽  
Health And Disease ◽  
In The Beginning ◽  
Cellular Pathology ◽  
Induced Changes ◽  
The Impact

In the mid-nineteenth century Virchow revolutionized pathology by introduction of the concept of “cellular pathology”. Today, a century later, this term has increasing significance in health and disease. We now are in the beginning of a new era in pathology, one which might well be termed “organelle pathology” or “subcellular pathology”. The impact of lysosomal diseases on clinical medicine exemplifies this role of pathology of organelles in elucidation of disease today.Another aspect of cell organelles of prime importance is their pathologic alteration by drugs, toxins, hormones and malnutrition. The sensitivity of cell organelles to minute alterations in their environment offers an accurate evaluation of the site of action of drugs in the study of both function and toxicity. Examples of mitochondrial lesions include the effect of DDD on the adrenal cortex, riboflavin deficiency on liver cells, elevated blood ammonia on the neuron and some 8-aminoquinolines on myocardium.

Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

1987 ◽  
Vol 45 ◽  
pp. 934-935
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda
Keyword(s):  
Cell Proliferation ◽  
Liver Function ◽  
Chronic Inflammation ◽  
Foam Cell ◽  
Term Effect ◽  
Short Term ◽  
Drug Induced ◽  
Experimental Induction ◽  
Tissue Alterations ◽  
Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

Drug-Induced Movement Disorders

2015 ◽  
Vol 25 (2) ◽  
pp. 70-77
Author(s):  
Amy Lustig ◽  
Cesar Ruiz
Keyword(s):  
Movement Disorders ◽  
Medical Management ◽  
Disease Process ◽  
Underlying Disease ◽  
Extrapyramidal Symptoms ◽  
Drug Induced ◽  
General Overview ◽  
Management Approaches ◽  
Broad Understanding ◽  
Underlying Disease Process

The purpose of this article is to present a general overview of the features of drug-induced movement disorders (DIMDs) comprised by Parkinsonism and extrapyramidal symptoms. Speech-language pathologists (SLPs) who work with patients presenting with these issues must have a broad understanding of the underlying disease process. This article will provide a brief introduction to the neuropathophysiology of DIMDs, a discussion of the associated symptomatology, the pharmacology implicated in causing DIMDs, and the medical management approaches currently in use.

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