Renal rupture

Ciprofloxacin (Cipro, Cipro XR, Proquin XR) [Antibiotic/ Fluoroquinolone] Uses Rx lower resp tract, sinuses, skin skin structure, bone/joints, urinary tract Infxns including prostatitis Action Quinolone antibiotic DNA gyrase Dose Adults. 250-750 mg PO ql2h XR 500-1000 mg PO q24h or 200-400 mg IV ql2h in renal impair Caution [C, /-] Children <18 y Contra Component sensitivity Disp Tabs, susp, inj SE Restlessness, N/V/D, rash, ruptured tendons, T LFTs Interactions T Effects Wf probenecid T effects OF diazepam, theophylline, caffeine, metoprolol, propranolol, phenytoin, warfarin effects W/ antacids, didanosine, Fe salts. Mg, sucralfate, Na bicarbonate,... 

Un, acute exacerbation of chronic bronchitis prophylaxis in transurethral procedures Action Quinolone antibiotic -1- DNA gyrase. Dose 400 mg/d PO X w/ renal insuff, avoid antacids Caution [C, —] Interactions w/ cation-containing products Contra Quinolone all gy, children <18 y,T QT interval, X Disp Tabs SE NA/ /D, abd pain, photosens, Szs, HA, dizziness, tendon rupture, periph al neuropathy, pseudomembranous cohtis, anaphylaxis Interactions t Effects W/ cimetidine, probenecid T effects OF cyclosporine, warfarin, caffeine X effects W/ antacids EMS Monitor ECG for TqT int val, esp in pts taking class lA/III antiarrhythmics monitor ECG and BP for signs of h5 povolemia and electrol5rte disturbances (hypokalemia) d/t D T risk of photosensitivity Rxns OD May cause NA /D, confusion and Szs symptomatic and supportive... 

Fluoroquinolones may damage growing cartilage and cause an arthropathy. Thus, these drugs are not routinely recommended for patients under 18 years of age. However, the arthropathy is reversible, and there is a growing consensus that fluoroquinolones may be used in children in some cases (eg, for treatment of pseudomonal infections in patients with cystic fibrosis). Tendinitis, a rare complication that has been reported in adults, is potentially more serious because of the risk of tendon rupture. Risk factors for tendonitis include advanced age, renal insufficiency, and concurrent... 

Figure 7.33 The renal accumulation and toxicity of gentamycin (G). Gentamycin is filtered in the glomerulus and enters the tubular lumen. Here, it is taken up by proximal tubular cells and in vesicles as part of the uptake process. These fuse with lysosomes (L) inside the cell. The accumulation of gentamycin inside the lysosome destabilizes it, causing it to rupture and release its hydrolytic enzymes (o). These cause damage within the cell. Also, gentamycin can directly damage mitochondria (M).

They act on the kidney by depressing the mechanisms that govern the active reabsorption of sodium and chloride ions. They are rapidly excreted by the kidney but their use is hazardous because their action is believed to be due to inorganic mercury ions released by rupture of the carbon-to-mercury bond, probably followed by the firm attachment of the mercury ion to a sulphydryl group of a renal enzyme. The administration of dimercaprol (SO), a strong chelating agent for mercury, removes mercury from the kidney and terminates the diuretic action. It is of interest that Paracelsus used calomel (mercurous chloride) as a diuretic. 

The endovascular procedure is most frequently used to treat infrarenal AAAs that are a leading cause of death in the older population, As our population ages, we will encounter AAAs more frequently than ever before. An aneurysm is defined by a size greater than 5 cm or 2.5 times the normal diameter of the native artery. Most aneurysms begin below the renal arteries and end close to the iliac bifurcation. More complicated AAAs exist involving the suprarenal aorta and visceral vessels and extending into the iliac arteries. The prevalence of AAAs is 3% to 10% for patients older than 50 years (I). They occur more frequently in men and reach a peak incidence close to the age of 80 years. AAA rupture is associated with an 80% to 90% mortality rate and therefore the focus of AAA treatment is on intervening before the aneurysm ruptures elective repair has mortality rate of less than 5%. 

Fransen GA, Vallabhaneni SR Sr, van Marrewijk CJ, et al, Rupture of infra-renal aortic aneurysm after endovascular repair a series from EUROSXAR registry, Eur J Vase Endovasc Surg 2003 26(5) 487-493. 

Cardiovascular diseases are the leading cause of death in the Western world. Basically, atherosclerosis manifests itself in three major organs and thereby leads to severe secondary diseases. Coronary disease results from atherosclerosis of the coronary arteries and culminates in myocardial infarction when vessels are occluded by a thrombus. In the brain, atherosclerosis gives rise to arterial thrombi or ruptures that result in a stroke. Atherosclerosis in the kidney leads to renal failure. Since these diseases significantly lower life expectancy, early recognition and elimination of risk factors (hypertension, diabetes mellitus, hyperlipidemia, and smoking) that promote atherosclerosis are essential. 

Complications Acute liver failure, arterioportal fistula formation, oesophageal varices (15) and pulmonary hypertension have been reported as complications. In most cases, the cause of death is anorexia with tumour cachexia, accompanied by signs of circulatory and renal failure. Occasionally, there is intraperitoneal haemorrhage, portal vein thrombosis (138,146) and tumour rupture with formation of haemorrhagic ascites. (121)... 

Other rare complications have been seldom reported, namely cryoglobulinemia with evidence of disseminated BCG infection (16), ruptured mycotic aneurysm of the abdominal aorta (17), bladder wall calcification (18), rhabdomyolysis (19), iritis or conjunctivitis with arthritis or Reiter s syndrome (20,21), and severe acute renal insufficiency due to granulomatous interstitial nephritis, which can occur even in the absence of other systemic complications (22). 

Tendinopathy and partial or complete tendon rupture as adverse events of fluoroquinolones have been reported during or shortly after the use of fluoroquinolones (80-84). Pefloxacin and ofloxacin have been implicated, as has ciprofloxacin (85,86). In six patients taking fluoroquinolones risk factors included renal insufficiency, glucocorticoid therapy, secondary hyperparathyroidism, advanced age, and diabetes mellitus (87). Cases have also been reported among immunocompromised renal transplant recipients (88). 

Old age, renal dysfunction, and concomitant corticosteroid therapy are predisposing risk factors (30,31). Tendon rupture occurred in less than four per million prescriptions (9). 

An 84-year-old man with diabetic nephropathy and end-stage renal disease began continuous ambulatory peritoneal dialysis and over the next year had four episodes of exit-site infection and peritonitis and used mupirocin ointment. The exit-site catheter became dilated and during an episode of infection for which he used mupirocin on 6 successive days, a longitudinal rupture developed in the peritoneal catheter, which was removed. The peritoneal liquid contained Escherichia coli and Proteus mirabilis and the catheter tip contained E. coli and Enterobacter cloacae. He was treated with ciprofloxacin, without complications, and after 1 month a new peritoneal catheter was inserted. 

A 67-year-old man underwent laparotomy for a ruptured abdominal aortic aneurysm (20). Postoperatively he was treated with hemodialysis because of acute renal insufficiency. Hyperkalemia was treated with sodium polystyrene sulfonate, after which he developed ulceration of the colon and required a hemicolectomy because of intractable blood loss. 

Toxicants that reduce ATP disrupt cell volume, ion concentrations, and cell polarity. Disruption of cell volume and ion homeostasis occurs by toxicant interaction with the plasma membrane increasing ion permeability or by attenuahng energy produchon. ATP depletion results in a decrease in Na, K -ATPase activity, resulting in cell swelling, and ultimately cell rupture [54, 55]. The tubular epithelia are polarized cells with specific transporters on the apical and basolateral domains. When a toxicant causes ATP depletion there is a dissociation of the Na, K -ATPase from the actin cytoskeleton and a redistribution from the basolateral to apical domain in the renal proximal tubule cells [56]. The loss of polarity of the cells disrupts the adhesion complexes and loss of cell-to-cell contact that facilitates further renal damage. 

Hyperkalemia may occur in acidosis, colitis, ruptured bladder and renal failure and in horses... 

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