Iopentol in patients with chronic renal failure: Its effects on renal function and its use as glomerular filtration rate parameter

Author(s):  
K. J. Berg ◽  
F. Kolmannskog ◽  
P. E. Lillevold ◽  
K. P. Nordal ◽  
L. Ressem ◽  
...  
1993 ◽  
Vol 85 (6) ◽  
pp. 733-736 ◽  
Author(s):  
R. Rustom ◽  
J. S. Grime ◽  
P. Maltby ◽  
H. R. Stockdale ◽  
M. J. Jackson ◽  
...  

1. The new method developed to measure renal tubular degradation of small filtered proteins in patients with normal renal function, using radio-labelled aprotinin (Trasylol) (R. Rustom, J. S. Grime, P. Maltby, H. R. Stockdale, M. Critchley, J. M. Bone. Clin Sci 1992; 83, 289–94), was evaluated in patients with chronic renal failure. 2. Aprotinin was labelled with either 99mTc (40 MBq) or 131I (0.1 MBq), and injected intravenously in nine patients, with different renal pathologies. 51Cr-EDTA clearance (corrected for height and weight) was 40 + 5.4 (range 11.2-81) ml min−1 1.73 m−2. Activity in plasma and urine was measured over 24–48 h, and chromatography on Sephadex-G-25-M was used to separate labelled aprotinin from free 99mTcO4− or 131I−. Renal uptake was measured for 99mTc-labelled aprotinin only. 3. The volume of distribution was 20.2 + 2.3 litres. Chromatography showed all plasma activity as undegraded aprotinin, and urine activity only as the free labels (99mTcO4− or 131I−). 4. As in patients with normal renal function, activity in the kidney appeared promptly, with 5.7 + 2.5% of the dose detected even at 5 min. Activity rose rapidly to 9.4 + 1.6% of dose after 1.5 h, then more slowly to 15.0 + 0.5% of dose at 4.5 h, and even more slowly thereafter, reaching 24.1 + 2.8% of dose at 24 h. Extra-renal uptake was again insignificant, and both 99mTcO4− and 131I− appeared promptly in the urine, with similar and uniform rates of excretion over 24 h. 5. Both tubular uptake at 24 h and the rate of tubular metabolism over 24 h were lower than in the patients with normal renal function studied previously, but only the rate of tubular metabolism was directly related to the glomerular filtration rate (r = 0.75, P <0.02). 6. Correction for the reduced glomerular filtration rate yielded values for both tubular uptake (0.67 + 0.14 versus 0.32 + 0.03% of dose/ml of glomerular filtration rate, P <0.005), and tubular metabolism (0.033 + 0.07 versus 0.015 + 0.001% of dose h−1 ml−1 of glomerular filtration rate, P <0.005) that were higher by comparison with those for patients with normal renal function studied previously. 7. Fractional renal degradation of 99mTc-aprotinin (in h−1), derived from the mean rate of urinary excretion of the free isotope over a given interval, divided by the mean cumulative kidney uptake over the same interval, also fell steeply early, and then more slowly to 0.07 + 0.01 h−1 at 14.25 h (between 4.5 and 24 h). 8. It is concluded that the method described previously is also suitable in patients with chronic renal failure, allowing further research into renal disease progression.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4592-4592
Author(s):  
Eugene Nikitin ◽  
Boldykyz Dzhumabaeva ◽  
Irina Kaplanskaya ◽  
Anait Melikyan ◽  
Ludmila Biryukova

Abstract Abstract 4592 The optimal treatment of patients with chronic lymphocytic leukemia (CLL) and concomitant renal impairment is unclear. Fludarabine containing regimens are contraindicated in patients with glomerular filtration rate less then 30 ml/min. Alkylating agents are either contraindicated or require dose reduction due to their relatively large renal clearance. Treatment choice is especially difficult in cases with refractoriness to alkylating drugs. The aim of this study was to assess safety and efficacy of bendamustine monotherapy in CLL patients with concomitant chronic renal failure. Seven patients with proven diagnosis of CLL and chronic kidney disease were treated with bendamustine monotherapy. The median age of patients was 66 years (range 61 – 83). All patients were males. The median creatinine level was 183 mkmol/L (range 165 – 573), the median level of glomerular filtration rate was 39 ml/min (range 23 – 47). The causes of chronic renal failure: membranous proliferative glomerulonephritis and focal CLL infiltration – 1 case, nephrectomy for cancer and massive CLL infiltration – 1 case, nephrectomy for cancer and pyelonephritis of sole kidney – 1 case, massive diffuse CLL infiltration with no other causes identified – 1 case, drug associated tubulointerstitial nephritis with development of irreversible renal failure – 1 case, chronic gout and urolithiasis in 1 case, unknown – 1 case. None of the patients required hemodialysis. Treatment consisted of bendamustine monotherapy, administered for two days every 4 weeks. Treatment in all patients started with dose 70 mg/m2/day. If the first course was well tolerated the dose was escalated to 100 mg/m2 on the next courses. Three patients were newly diagnosed and four patients had relapsed disease, after a medium of 2 lines of therapy (range 1 – 2). Two patients were refractory to alkylating drugs. Before initiation of bendamustine 4 patients had Binet stage C, and 3 Binet stage B. Four patients received all planned 6 cycles of therapy with dose escalation to 100 mg/m2/day. In three patients treatment was stopped prematurely. In one patient treatment was discontinued after the 4th cycle because of the grade III skin rush and grade II polyneuropathy. One severely cardio compromised patient of 72 years developed grade III bradicardia after first cycle, requiring installation of cardiac pacemaker. One patient of 83 years with refractoriness to previous treatment died after 2 cycles from infectious complications. Neutropenia grade III was observed in 5 cycles in 3 patients. Aggravation of thrombocytopenia (grade II) was observed in 2 patients and aggravation of anemia (grade I) in 3 patients. In no case there was worsening of renal function. Decrease of creatinine and urea level was observed in 5 patients. Response can be evaluated in 5 patients. 2 patients achieved a nodular PR, and 3 patients achieved a PR. In conclusion, monotherapy with bendamustine can be safely used in patients with CLL and renal impairment. Doses up to 100 mg/m2 are tolerated and do not cause worsening of renal function or severe hematological toxicity. Disclosures: No relevant conflicts of interest to declare.


1975 ◽  
Vol 49 (3) ◽  
pp. 193-200 ◽  
Author(s):  
C. H. Espinel

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.


Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghan

Acute renal failure (also referred to as acute kidney injury) refers to a rapid decrease in renal function; it is reflected by an increase in blood urea and creatinine and is often associated with oliguria (a urine volume of less than 400 ml/24 hours). It usually develops over days to weeks. Acute kidney injury has been variously classified, but the current classifications are based on the glomerular filtration rate (or creatinine), looking at changes from baseline, and the presence of oliguria or anuria. The potential etiologies of acute kidney injury are usually considered anatomically under the headings prerenal, renal (intrinsic), and postrenal. This chapter looks at the etiology, symptoms, clinical features, demographics, complications, diagnosis, and treatment of acute kidney injury.


Jurnal NERS ◽  
2017 ◽  
Vol 9 (1) ◽  
pp. 43 ◽  
Author(s):  
Martono Martono ◽  
Satino Satino

Introductions: Hemodialysis is often interpreted incorrectly. People assume that the action is an action that will cure the treatment of hemodialysis patients with renal failure after hemodialysis. The purpose of this study was to determine the ability of critical changes in renal glomerular fi ltration rate in patients with hemodialysis nursing care. Method: The design is quasi-experimental study carried out 2 times the observation that pre-test and post-test with a retrospective approach. The study population was all patients who underwent hemodialysis with a sample size of 33 respondents. Analysis of the research data using the paired t test. Result: The results of this study indicate that the glomerular fi ltration rate fi xing Hemodialysis towards better able to detect and prevent the severity of renal function as evidenced by the value of P = 0.031 for change 9.18. Discussion: Hemodialysis fi x glomerular fi ltration rate towards better able to detect and prevent the severity of renal function with the ability to take into account the age and sex and weight stability. All the patients with chronic renal failure in the terminal stage are expected to follow and adhere to regular hemodialysisprogram with regard stabilization weight, age, and sex in order to avoid the severity of kidney function worse.Keyword: Glomerular Filtration Rate, Hemodialysis, Severity of Kidney Function


Author(s):  
Debra Ugboma ◽  
Helen Willis

The aim of this chapter is to provide nurses with the knowledge to be able to assess, manage, and care for people with the renal disorders chronic kidney disease (CKD) and acute kidney injury (AKI) in an evidence-based and person-centred way. In recent years, AKI has replaced the term ‘acute renal failure’. The chapter will provide a comprehensive overview of the causes, risk factors, and impact of CKD and AKI, before exploring best practice to deliver care, as well as to prevent further progression of these conditions. Nursing assessments and priorities are highlighted throughout, and further nursing management of some of the symptoms and common health problems associated with CKD and AKI can be found in Chapters 6, 9, 15, and 19, respectively. Chronic kidney disease (CKD) is the gradual and usually permanent loss of some kidney function over time (Department of Health, 2007). In CKD, the damage and decline in renal function usually occurs over years, and in early stages can go undetected (Department of Health, 2005a). CKD has rapidly moved up the healthcare agenda in recent years, primarily because of the links with cardiovascular risk, and with a shift in focus away from the treatment of established renal failure towards the detection and prevention of CKD in primary care (O’Donohue, 2009). Glomerular filtration rate (GFR) is an indicator of renal function and is the rate at which blood flows through, and is ‘filtered’ by, the kidney; a normal GFR is approximately 125 ml/min. CKD is classified into five stages according to an estimated glomerular filtration rate (eGFR) and, in the milder stages, further evidence of renal damage such as proteinuria and haematuria. This classification holds regardless of the underlying cause of kidney damage. The understanding of GFR is pivotal to caring for patients with renal disorders. Monitoring, management, and referral of the patient in the earlier stages of CKD became much clearer following the publication of the National Clinical Guidelines for the Management of Adults with Chronic Kidney Disease in Primary and Secondary Care (NICE, 2008a). Many people with stage 3 CKD, unless they have proteinuria, diabetes, or other comorbidity such as cardiovascular disease, have a good prognosis and can be managed in primary care (Andrews, 2008).


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