Effects of I ,25-Dihydroxyvitamin-D3 on Renal Function, Mineral Balance, and Growth in Children with Severe Chronic Renal Failure

To confirm and extend previous observations of enhanced linear growth in children with chronic renal disease being treated with 1,25-dihydroxyvitamin- D3 and to characterize further the calcium, phosphorus, magnesium, and zinc disorders in renal failure, 11 children (mean age 8 ± 5 years) with chronic renal insufficiency (glomerular filtration rate 18% ± 13% of normal) were evaluated on the basis of their reciprocal serum creatinine concentrations, height-velocity curves, mineral balances, and radiologic findings. Reciprocal serum creatinine concentrations analyzed retrospectively and prospectively during 32 months of 1,25-dihydroxyvitamin-D3 therapy showed progression of renal failure at rates linearly identical with those before treatment, thus suggesting that the treatment did not accelerate the rate of deterioration of glomerular filtration rate in chronic renal insufficiency. Indeed, one patient manifested a lesser decline in renal function (P sjlt .05). The height velocity of six of the children (75%) less than 12 years of age improved markedly over that expected for chronologic and bone ages after one year of treatment with orally administered 1,25-dihydroxyvitamin-D3, 15 to 35 ng/kg/day. All other medications except vitamin D2 were continued at their pretreatment dosage levels throughout the study. Growth velocity was unimproved in two of three children older than 12 years at the initiation of 1,25-dihydroxyvitamin- D3 therapy. Mineral balance data showed significant retention of calcium, phosphorus, magnesium, and zinc (357 ± 32 mg/sq m/day, 250 ± 82 mg/sq m/day, 38 ± 32 mg/sq m/day, and 1,157 ± 283 µ/sq m/day, respectively), after treatment for 12 months. In addition, serum calcium, alkaline phosphatase, and parathyroid hormone concentrations returned toward normal. Finally, healing of renal osteodystrophy was radiologically evident after six months of therapy.

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Hypercalcemia in Children with Disorders of Calcium and Phosphate Metabolism During Long-Term Treatment with 1,25-Dihydroxyvitamin-D3

PEDIATRICS ◽

10.1542/peds.72.2.225 ◽

1983 ◽

Vol 72 (2) ◽

pp. 225-233

Author(s):

James C. M. Chan ◽

Reuben B. Young ◽

Uri Alon ◽

Peter Mamunes

Keyword(s):

Renal Function ◽

Calcium Phosphate ◽

Renal Insufficiency ◽

Hypophosphatemic Rickets ◽

Phosphate Metabolism ◽

Dihydroxyvitamin D3 ◽

1,25 Dihydroxyvitamin D3 ◽

Renal Function Deterioration ◽

Calcium And Phosphate Metabolism ◽

1,25 Dihydroxy Vitamin D3

Forty-two children received 1,25-dihydroxy-vitamin-D3 for treatment of disorders in calcium and phosphate metabolism secondary to chronic renal insufficiency (n = 29), sex-linked dominant hypophosphatemic rickets (n = 9), hypoparathyroidism (n = 2), and pseudohypoparathyroidism (n = 2). Serum calcium, phosphate, and creatinine concentrations were measured monthly for a mean of 26 months and a total of 1,079.5 patient-months. Patients with renal osteodystrophy manifested hypercalcemia (>11 mg/dL) once in every 13 months of treatment on the average. Of three children with hypophosphatemic rickets who experienced hypercalcemia, two proved to have tertiary hyperparathyroidism. Among children with hypoparathyroidism and pseudohypoparathyroidism, three episodes of hypercalcemia were observed during 124.5 patient-months, an incidence of one hypercalcemic episode per 39 treatment months. Renal function, as represented by reciprocals of serum creatinine determined retrospectively for a mean of 22 months before and prospectively for a mean of 26 months after initiation of 1,25-dihydroxyvitamin-D3 treatment, underwent no significant changes except in seven of 29 children with chronic renal insufficiency, six of whose rate of renal function deterioration increased on the treatment and one whose rate decreased. With one exception, hypercalcemia was associated in all cases with accelerated renal function deterioration. Before and after initiation of treatment with 1,25-dihydroxyvitamin-D3 the mean calcium x phosphate solubility products were 42.9 and 47.2, respectively. Values less than 60 are accepted as normal. Hypercalcemia is an occasional concomitant of such treatment and a more rapid deterioration of renal function may occur in some of the patients treated with 1,25-dihydroxyvitamin-D3. Thus, careful monitoring of concentrations of serum calcium, phosphate, and creatinine must accompany 1,25-dihydroxy-vitamin-D3 therapy.

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Acute kidney injury

10.1093/med/9780199568741.003.0162 ◽

2018 ◽

Author(s):

Aron Chakera ◽

William G. Herrington ◽

Christopher A. O’Callaghan

Keyword(s):

Acute Kidney Injury ◽

Renal Failure ◽

Renal Function ◽

Acute Renal Failure ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Filtration Rate ◽

Urine Volume ◽

Kidney Injury ◽

Rapid Decrease

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.

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Renal Insufficiency and Failure

Hematology ◽

10.1182/asheducation-2010.1.431 ◽

2010 ◽

Vol 2010 (1) ◽

pp. 431-436 ◽

Cited By ~ 16

Author(s):

Meletios A. Dimopoulos ◽

Evangelos Terpos

Keyword(s):

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Renal Impairment ◽

Renal Disease ◽

Renal Injury ◽

Filtration Rate ◽

Acute Renal Injury ◽

Sustained Improvement ◽

Definition Of

Abstract Renal impairment is a common complication of multiple myeloma. Chronic renal failure is classified according to glomerular filtration rate as estimated by the MDRD (modification of diet in renal disease) formula, while RIFLE (risk, injury, failure, loss and end-stage renal disease) and AKIN (acute renal injury network) criteria may be used for the definition of the severity of acute renal injury. Novel criteria based on estimated glomerular filtration rate measurements are proposed for the definition of the reversibility of renal impairment. Renal complete response (CRrenal) is defined as sustained (i.e., lasting at least 2 months) improvement of creatinine clearance (CRCL) from under 50 mL/min at baseline to 60 mL/min or above. Renal partial response (PRrenal) is defined as sustained improvement of CRCL from under 15 mL/min at baseline to 30 to 59 mL/min. Renal minor response (MRrenal) is defined as sustained improvement of the baseline CRCL of under 15 mL/min to 15 to 29 mL/min or, if baseline CRCL was 15 to 29 mL/min, improvement to 30 to 59 mL/min. Bortezomib with high-dose dexamethasone is considered the treatment of choice for myeloma patients with renal impairment and improves renal function in most patients. Although there is limited experience with thalidomide, this agent can be administered at the standard dosage to patients with renal failure. Lenalidomide, when administered at reduced doses according to renal function, is effective and can reverse renal impairment in a subset of myeloma patients.

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Renal Tubular Protein Degradation of Radiolabelled Aprotinin (Trasylol) in Patients with Chronic Renal Failure

Clinical Science ◽

10.1042/cs0850733 ◽

1993 ◽

Vol 85 (6) ◽

pp. 733-736 ◽

Cited By ~ 9

Author(s):

R. Rustom ◽

J. S. Grime ◽

P. Maltby ◽

H. R. Stockdale ◽

M. J. Jackson ◽

...

Keyword(s):

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Chronic Renal Failure ◽

Glomerular Filtration ◽

Normal Renal Function ◽

Filtration Rate ◽

Renal Uptake ◽

The Mean ◽

Renal Tubular

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.

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Severity Renal Function Detection through Critical Changes Glomerular Filtration Rate in Hemodialysis Patients

Jurnal NERS ◽

10.20473/jn.v9i1.2963 ◽

2017 ◽

Vol 9 (1) ◽

pp. 43 ◽

Cited By ~ 1

Author(s):

Martono Martono ◽

Satino Satino

Keyword(s):

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Kidney Function ◽

Filtration Rate ◽

Hemodialysis Patients ◽

Quasi Experimental ◽

Fi Ltration ◽

Age And Sex

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

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Estimated Glomerular Filtration Rate Changes In Patients (Pts) With Chronic Myeloid Leukemia (CML) Treated With Tyrosine Kinase Inhibitors (TKI)

Blood ◽

10.1182/blood.v122.21.1488.1488 ◽

2013 ◽

Vol 122 (21) ◽

pp. 1488-1488 ◽

Cited By ~ 4

Author(s):

Musa Yilmaz ◽

Hagop M. Kantarjian ◽

Alfonso Quintas-Cardama ◽

Susan O'Brien ◽

Jan A. Burger ◽

...

Keyword(s):

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Research Funding ◽

Filtration Rate ◽

Estimated Glomerular Filtration Rate ◽

Estimated Gfr ◽

Free Survival ◽

Tki Treatment

Abstract Introduction TKI are standard therapy for pts with CML. Although generally safe, they are associated with some adverse events, most of them manageable and transient. Renal dysfunction has been reported anecdotally on pts with CML treated with TKI. We investigated the incidence of acute renal failure (ARF) and chronic renal failure (CRF) among the CML pts treated with TKI, and analyzed possible relationship between treatment duration with TKI and changes in estimated glomerular filtration rate (GFR). Methods Four hundred and seventy-five pts treated with imatinib (255 pts; 49 at 400 mg daily; 206 at 800 mg daily), dasatinib (101 pts) and nilotinib (119 pts) in prospective clinical trials at a single institution were evaluated. Pts were followed routinely with blood chemistries including renal function tests, at least weekly during the first 2-3 months, then every 2-4 weeks for 6-12 months, then every 8-12 weeks. GFR was estimated using the Modification of Diet in Renal Disease (MDRD) equation and recorded from the onset of TKI treatment until last follow up. ARF was defined as an increase in serum creatinine of ≥0.3 mg/dl, and CRF defined as an estimated GFR ≤ 60 ml/min/1.73 m2 persisting for at least 90 days. Results After a median follow-up of 50 months (range, 2 to 138 months), 19 pts (4%) developed ARF. The median time of onset for ARF was 9 days (range 4-84 days). Sixteen of 19 pts (84%) were on imatinib, 2 on nilotinib, and 1 on dasatinib (p=0.006). There was no association between imatinib dose and incidence of ARF (2% with 400mg vs 7% with 800mg) (p=0.174). The median age for pts with ARF was 58 yrs compared to 48 for pts with no ARF (p=0.009). Seventy-nine percent (15 out of 19) of ARF pts and 59% (269 of 456) of pts without ARF were male (p=0.063). During study time, estimated GFR decreased significantly in pts treated with imatinib compared to dasatinib (Figure 1) (p<0.001). Interestingly, in pts treated with nilotinib, we observed significant increase in GFR when we compare baseline GFR to the GFR in all other time points (p<0.05). 442 pts (94%) had no CRF at baseline, and 48 of these pts (11%) developed CRF over the course of TKI treatment. Among them, 39 pts (81%) were on imatinib compared to 19% on other TKIs (5 dasatinib, 4 nilotinib) (p<0.001). There was no association between imatinib dose (400mg and 800mg) and CRF incidence (p=0.591). The median age for pts who developed CRF was 61 yrs compared to 47 for those with no CRF (p=<0.001). Fifty-eight percent (28 out of 48) of CRF pts and 60 % (256 of 427) of pts without CRF were male (p=0.828). Overall CCyR rate was the same (89%) in pts who had ARF and no ARF, and overall MMR rate was 79% in pts with ARF and 83% in pts with no ARF (p=0.401). Overall CCyR rate was 98% in pts who developed CRF over the course of TKI therapy compared to 89% in pts who did not develop CKD (p=0.026). Similarly, overall MMR rate was higher (96%) in pts developed CKD compared to pts who did not have CKD (82%) (p=0.013). Overall survival and transformation free survival was not statistically different when compared pts with ARF vs no ARF and CRF vs no CRF. However, pts with ARF had decreased event free survival (EFS) when compared to no ARF pts (p=0.019). There was no EFS difference in CRF pts (0.966). Conclusion Long-term treatment with imatinib may cause a significant decline in estimated GFR. Interestingly, treatment with nilotinib may cause a slight improvement in GFR. It is important that pts are monitored for renal function during therapy with TKI, with particular attention to those with risk factors for renal dysfunction. Disclosures: Ravandi: Pfizer and Novartis: Honoraria; BMS: Research Funding. Jabbour:Novartis, BMS, Ariad, and Pfizer: Consultancy. Cortes:Ariad, BMS, Novartis, Pfizer and Teva: Research Funding; BMS, Pfizer and Teva. : Consultancy.

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Understanding Renal Disorders

Adult Nursing Practice ◽

10.1093/oso/9780199697410.003.0021 ◽

2012 ◽

Author(s):

Debra Ugboma ◽

Helen Willis

Keyword(s):

Primary Care ◽

Chronic Kidney Disease ◽

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Kidney Disease ◽

Glomerular Filtration ◽

Filtration Rate ◽

Renal Disorders ◽

Department Of Health

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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Renal Endothelin System in Obstructive Jaundice: Its Role in Impaired Renal Function of Bile-Duct Ligated Rats

Clinical Science ◽

10.1042/cs0920579 ◽

1997 ◽

Vol 92 (6) ◽

pp. 579-585 ◽

Cited By ~ 21

Author(s):

Herbert J. Kramer ◽

Kriemhild Schwarting ◽

Angela Backer ◽

Harald Meyer-Lehnert

Keyword(s):

Renal Failure ◽

Renal Function ◽

Acute Renal Failure ◽

Glomerular Filtration Rate ◽

Bile Duct ◽

Obstructive Jaundice ◽

Glomerular Filtration ◽

Filtration Rate ◽

Kidney Weight ◽

Duct Ligation

1. Obstructive jaundice predisposes the kidney to acute renal failure. Endothelin (ET), a potent renal vasoconstrictor and modulator of the tubular action of arginine vasopressin, has been suggested to play a pathogenetic role in acute renal failure. In the present study we therefore investigated renal function and the renal ET system in rats on day 4 after bile-duct ligation (BDL) or sham-operation (SO), without (n = 7 in each group) and with treatment with bosentan, a combined ETA/ETB receptor blocker, (n = 5 in each group). 2. On day 4 after BDL, serum bilirubin had increased to 226 ± 10 μmol/l (SEM) as compared with 6 ± 2 μmol/l in SO rats. Endogenous creatinine clearance, an index of glomerular filtration rate, was significantly reduced to 0.7 ± 0.1 ml min−1 g−1 of kidney weight after BDL as compared with 1.1 ± 0.1 ml min−1 g−1 of kidney weight after SO (P < 0.05). Bosentan prevented the decrease in glomerular filtration rate (1.0 ± 0.2 ml min−1 g−1 of kidney weight), as well as polyuria and defective concentrating ability, in BDL rats. 3. Plasma ET concentration on day 4 after surgery (28.2 ± 1.5 pmol/l) was higher (P < 0.01) in BDL than in SO rats (12.9 ± 1.5 pmol/l) and rose further in bosentan-treated BDL and SO rats (43.4 ± 5.1 compared with 21.9 ± 6.6 pmol/l). Urinary ET excretion was significantly higher in BDL rats than in SO rats (1.58 ± 0.22 compared with 1.28 ± 0.18 pmol 24h−1 100 g−1 of body weight; P < 0.05). 4. ET synthesis by glomeruli isolated from BDL rats was lower [81 ± 19 fmol h−1 (mg of protein)−1] than that from SO-rats [139 ± 28 fmol h−1 mg of protein)−1; P < 0.05], whereas papillary ET synthesis was higher in BDL [10 ± 3 fmol h−1 (mg of protein)−1] than in SO rats [4 ± 1 fmol h−1 (mg of protein)−1; P < 0.05]. 5. The results indicate that BDL is associated with increased plasma ET concentration and suppression of GFR. Enhanced renal inner medullary collecting-duct ET synthesis, which is reflected by increased urinary ET excretion, may reduce distal tubular water absorption in BDL rats. Increased circulating and renal papillary ET synthesis may thus contribute to renal dysfunction and predispose the kidney to acute renal failure in obstructive jaundice.

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Effects of IGF-I on renal function in patients with chronic renal failure

AJP Renal Physiology ◽

10.1152/ajprenal.1993.264.5.f917 ◽

1993 ◽

Vol 264 (5) ◽

pp. F917-F922 ◽

Cited By ~ 1

Author(s):

M. H. O'Shea ◽

S. B. Miller ◽

M. R. Hammerman

Keyword(s):

Renal Failure ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Plasma Flow ◽

Filtration Rate ◽

Renal Plasma Flow ◽

Kidney Volume ◽

Igf I ◽

Reduced Renal Function

Insulin-like growth factor I (IGF-I) has been shown to increase glomerular filtration rate and renal plasma flow in rats and humans with normal renal function. However, rats with reduced renal function are resistant to these effects. To determine whether IGF-I affects glomerular filtration rate and renal plasma flow in humans with reduced renal function, we administered recombinant human IGF-I (rhIGF-I) to patients with moderate chronic renal failure. Four patients whose baseline inulin clearances were 21.9, 23.2, 34.9, and 55.1 ml.min-1.1.73 m-2 were placed on a 1 g.kg-1.day-1 protein diet and studied over a 10-day period (0-10). On days 4-7, 100 micrograms/kg of rhIGF-I was subcutaneously administered twice daily to the patients. The effects of rhIGF-I on levels of circulating IGF-I, inulin clearance, p-aminohippurate (PAH) clearance, kidney volume, plasma glucose, plasma and urine calcium and phosphate, and urine sodium and protein were determined. Administration of rhIGF-I increased levels of circulating IGF-I, inulin clearances, PAH clearances, and kidney size in each of the four patients receiving the growth factor. IGF-I did not cause weight gain, natriuresis, proteinuria, or hypoglycemia. Plasma calcium and phosphate were not affected by rhIGF-I. However, the percent tubular reabsorption of filtered phosphate was increased. We conclude that administration of rhIGF-I can enhance glomerular filtration rate and renal plasma flow at least in some humans with moderately reduced renal function. The enhancement is associated with an increase in kidney volume.

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