Urinary creatinine levels

RISK FOR INEFFECTIVE TISSUE PERFUSION RENAL When the patient is taking a drag tiiat is potentially toxic to die kidneys, die nurse must carefully monitor fluid intake and output. In some instances, die nurse may need to perform hourly measurements of die urinary output. Periodic laboratory tests are usually ordered to monitor the patient s response to therapy and to detect toxic drag reactions. Seram creatinine levels and BUN levels are checked frequentiy during the course of therapy to monitor kidney function. If the BUN exceeds 40 mg dL or if the serum creatinine level exceeds 3 mg cIL, the primary health care provider may discontinue the drug therapy or reduce the dosage until renal function improves. 

Blood lead levels, urinary lead levels, serum creatinine, blood urea nitrogen (BUN), creatinine clearance (CCT), and NAG were measured in 158 male and 51 female workers in a lead battery factory or a lead smelting plant in Japan (Ong et al. 1987). Controls consisted of 30 professional and laboratory staff members with no history of renal disease or lead exposure. The length of exposure to lead averaged 10.8 8.0 years with a range of 1-36 years. Exposure levels were not available, but indicators of lead body burden in the exposed workers were PbB level = 3.0-80.0 pg/dL and urinary lead level =... 

A report entitled Chemical Trespass was issued in May 2004 by the Pesticide Action Network (Schafer et al., 2006). It contained detailed analysis of 2000/01 National Health and Nutrition Examination Survey (NHANES) OP urinary metabolite data and used published methods to estimate exposure levels to parent compounds from creatinine corrected urinary metabolite levels. They focused on chlorpyrifos and its metabolite 3,4,6-trichloro-2-pyridinol (TCP), and found that chlorpyrifos exposures for children ages 6-11 and 12-19 exceeded EPA s chronic population-adjusted dose (cPAD) by surprisingly wide margins. Geometric mean TCP levels were 3 to 4.6 times higher than the EPA-estimated safe dose, as shown in Fig. 14.2. The more heavily exposed children received daily doses more than ten times the safe level. 

White Phosphorus. No changes in urinary creatinine levels were observed in workers exposed to an unspecified amount of airborne white phosphorus (Hughes et al. 1962). Evidence of severe renal effects have been observed in humans orally exposed to white phosphorus and burned by white phosphorus. In animals, renal effects have been observed following oral and dermal burn exposure. There is no information on the potential of white phosphorus to induce renal effects in humans dermally exposed to white phosphorus or animals exposed by inhalation and dermal routes. 

A 24-year-old man (Patient 3). This patient had flu-like symptoms, and took a mixed preparation consisting of bucetin at 120 mg and aspirin at 240 mg. After 15 h, he participated in a 200-m race in an athletics meeting (October 10, 1980). After 6h, he attended our hospital with nausea and bilateral loin pain. The severe pain, which made it impossible for him to drive a car, persisted for 2 days. His serum creatinine and urinary protein levels were 2.4mg/dl and 2+, respectively, 4 days after onset. The patient was negative for urinary occult blood, and his urinary sodium level was 99mEq/l. On the same day, drip infusion pyelography (DIP) revealed no ureteral... 

This patient, who had autosomal dominant polycystic kidney disease (ADPKD), almost drowned and then developed ALPE. On July 20, 1990, he nearly drowned in the sea at 1500 hours, and was brought to our hospital by ambulance for dyspnea and severe loin pain at 1620 hours. On admission, metabolic acidosis was observed. His CRP, serum creatinine, CPK, amylase, and urinary protein levels were 1+, 1.5mg/dl, 116 U/l, 592IU/1 (derived from the salivary gland), and 2+, respectively. His body temperature was 37.7°C, and his blood pressure was 110/60 mmHg. His pulse and respiratory rate were 120/min and 22/min, respectively. Delayed CT 6h after the administration of contrast medium showed wedge-shaped contrast enhancement in the noncystic renal parenchyma (Fig. 34). On July 24, a bone scan with MDP revealed patchy lesions (Fig. 35). His serum creatinine level was 1.3 mg/dl, which had decreased to 1.0 mg/dl on July 27. The patient was then discharged. 

Fig. 65. Relationship between urinary 8-isoprostane and serum creatinine levels. In the initial phase, when the serum creatinine level was high, there was no increase in urinary 8-isoprostane. In the recovery phase, the urinary 8-isoprostane level increased...

Urine samples collected from two human subjects, prior to (minus 24 to 0 hours) and after (plus 2 to 6 hours) oral administration of 30 mg A9-THC, were hydrolyzed and extracted as described in the experimental section. Pre- and post-drug extracts corresponding to equivalent urinary creatinine levels were separated by reverse phase HPLC. The pre-drug extract was used as a... 

It is difficult to obtain an accurate measure of renal function in patients with cirrhosis. A number of studies have shown that they tend to have low serum creatinine levels. This has been explained by a reduced muscle mass in cirrhotic patients and a reduced conversion of creatine to creatinine [10]. The calculation of creatinine clearance using the Cockcroft and Gault formula is also inaccurate in predicting GFR in these patients because it uses the serum creatinine level (which may be falsely low) and body weight in the calculation, which is likely to be inflated due to the presence of ascites [12]. The measured creatinine clearance, based on urinary excretion of creatinine, should theoretically be more accurate, even in patients with reduced muscle mass or impaired creatinine synthesis. However, it has been shown that this also overestimates the GFR because of an increased fractional tubular secretion of creatinine in cirrhotic patients, particularly those with reduced GFR [10]. 

Creatinine, a notable exception, is not reabsorbed by the tubules. All of the creatinine entering Bowman s space enters the bladder, without being reabsorbed and reentering the bloodstream. The amount of creatinine found in the urine thus accurately reflects the GFR. Tn medical practice, plasma and urinary creatinine levels are used on a day-to-day basis for detection of renal diseases. Figure 4JJ7, a diagram of the glomerulus, illustrates the flow of fluids to the urinary bladder. 

Most authors define CMIN by an increase of serum creatinine of more than 1 mg/ dl 2-3 days after CM exposure. Other reasons for an acute deterioration of renal function have to be excluded. Some investigators even believe that a lower increase of serum creatinine (0.5 mg/ dl 2-4 days after CM) also should be classified as CMIN. It would also be prudent to look for a fall of GFR (general >25% from basehne) with more sensitive methods (i.e. inuhn clearance, iothahnate clearance, iohexol clearance [7. Next to changes in GFR or serum creatinine levels an increase in urinary enzyme excretion seems to also be a sensitive marker of tubular damage after CM exposure [7, 8]. However, no conclusive relationship has been demonstrated between the detection of enzymes in urine and the fall in GFR [8-11]. 

A common problem in urine levels is the dilution. In case of Cd in urine, levels generally are given corrected for creatinine or urinary density. 

Side effects and adverse reactions include flushing, fever, chills, nausea, vomiting, hypotension, paresthesias, and thrombophlebitis. It is highly toxic, causes nephrotoxicity and electrolyte imbalance, especially hypokalemia (low potassium) and hypomagnesemia (low serum magnesium). Urinary output, BUN, and serum creatinine levels should be closely monitored. 

Urinary tract A case report was published on anti-neutrophil cytoplasmic antibody (ANCA)-positive pauci-immxme glomerulonephritis during febuxostat treatment. A 63-year-old African started treatment with febuxostat (dose not reported) because he had a history of chronic asymptomatic hyperuricemia which was not adequately controlled by allopurinol therapy. After 6 months of febuxostat therapy he developed AKI, characterised by acute renal failure, nephritic syndrome, proteinuria, microscopic haematuria and aseptic leukocyturia. Within 48 h after discontinuation of febuxostat, serum creatinine levels improved, although nephritic syndrome remained. ANCA-positive pauci-immune glomerulonephritis was confirmed by renal biopsy revealing diffuse crescentic necrotizing glomerulonephritis [60 ]. 

A retrospective case-control study of the effect of ceftriaxone on the urinary concentration of calcium included 103 patients who were treated for bacterial pneumonia. The patients were divided into groups depending on which antibiotic they received. Calcium and creatinine levels in serum and urine were collected before and after treatment, and the urinary calcium to creatinine ratios (uCa/Cr mg/mg) were calculated. There was a significant difference when comparing the uCa/Cr ratio in the ceftriaxone group to that of the amoxicillin group after treatment. These results showed that ceftriaxone increases the urinary excretion of calcium, and therefore may increase the risk of urolithiasis. The authors suggest that levels of uCa/Cr should be measured in patients in order to prevent this [70 ]. 

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