To examine the independent relationship between obesity, as estimated by body mass index (BMI), and progression of chronic kidney disease. We hypothesized that BMI would be associated with decline in estimated glomerular filtration rate (eGFR), independent of diabetes mellitus, hypertension, and other risk factors for progression of chronic kidney disease.
A retrospective cohort study was carried out.
The study was carried out at Nephrology ambulatory clinics of the London Health Sciences Centre, Canada.
The study included incident and prevalent patients with eGFR
Diabetic nephropathy develops in about 45% of insulin dependent diabetics of whom two-thirds will develop renal failure, the rest dying from cardiovascular disease. Most of the excess mortality of insulin dependent diabetics occurs in those with proteinuria. Among non-insulin dependent diabetics nephropathy is also an important cause of increased mortality but this is mainly from cardiovascular disease. Once diabetic nephropathy is established it progresses relentlessly to end-stage renal failure over about seven years, but ranging from five to 20 years. The explanation for the different rates of progression in individual patients is not understood. Hypertension accompanies diabetic nephropathy and its treatment may retard the progression of renal failure. Other forms of intervention include glycaemic control which has not been shown to have any effect, and protein restriction for which no conclusions can be drawn at present. The diagnosis of diabetic nephropathy is straightforward in the presence of a typical history and clinical features. Non-diabetic renal disease is sometimes the cause of renal failure and may require specific treatment; prognosis for renal failure treatment may be better than for nephropathy patients with other diabetic complications. Other diabetic complications develop as diabetic nephropathy progresses, most notably cardiac and peripheral vascular disease. Proliferative retinopathy and neuropathy are considerable problems and their management needs attention both before and after renal failure treatment.
Seventy-five patients with congenital nephrotic syndrome of Finnish type were identified in Finland in the period 1965-1973, giving an incidence of 12-2/10(5). A large placenta and proteinuria from birth are the hallmarks of the disease. About one-quarter of the patients had oedema and/or abdominal distension at birth and in all cases the full nephrotic syndrome was documented before 2 months. More than half of the patients died before 6 months and none lived longer than 2 years 3 months. A slight rise in blood urea nitrogen or serum creatinine levels occurred in 14 cases, but in none of these did a frank uraemia develop before death. Infection appeared to be the immediate cause of death in 31% of the cases; in 43% no cause of death other than congenital nephrotic syndrome could be shown. Thrombi in large vessels were found in 11 out of 58 necropsies.
Cites: Ann Paediatr Fenn. 1962;8:181-814035149
Cites: Ann Paediatr Fenn. 1956;2(3):227-4113373132
Cites: Am J Med. 1974 Apr;56(4):565-94818421
Cites: Am J Obstet Gynecol. 1972 Nov 1;114(5):595-84118006
To evaluate the predictability of eclampsia and explore the role for seizure prophylaxis in a population with a low frequency of seizure prophylaxis.
A retrospective review was conducted of all women with eclampsia registered at the Foothills Hospital in Calgary, Alberta, between 1991 and 2000. The data collected included timing of seizure in relation to diagnosis of gestational hypertension (GHTN) and delivery, method of seizure prophylaxis (if any), and maternal characteristics.
During the study period, 3075 of 38,577 women (8.0%) were diagnosed with GHTN, with or without proteinuria or adverse conditions. Three percent had received magnesium sulfate for seizure prophylaxis. Of these 3075 women, 17 (0.6%) developed eclampsia, none of whom was receiving magnesium sulfate for seizure prophylaxis at the time. Of these, 10 women (59%) exhibited GHTN prior to their first seizure, including 6 women with GHTN with adverse conditions, 3 with GHTN with proteinuria but without adverse conditions, and 1 with GHTN without proteinuria or adverse conditions. Five of the 17 women had seizures that occurred prior to labour, 6 were intrapartum, and 6 were postpartum. Nine (53%) of the 17 women with eclampsia had their initial seizure after the diagnosis of GHTN and before 24 hours postpartum.
Seizure prophylaxis for all the women with GHTN, from the time of diagnosis through 24 hours postpartum, may have been able to prevent as many as 53% of eclamptic episodes. Three hundred and seven women with GTHN would have to receive seizure prophylaxis to prevent one seizure.
We followed 1,134 patients with Type 1 (insulin-dependent) diabetes, diagnosed between 1933 and 1952, until 1982 or death or until their emigration. Their age at onset of diabetes was under 31 years. Information concerning the development of persistent proteinuria was sought in every case. In 104 cases, the data were either questionable or the patient could not be traced. Twenty-nine patients developed non-diabetic proteinuria. Among the remaining 1,001 patients, 406 developed persistent proteinuria (350 died) and 595 did not (166 died). The incidence of persistent proteinuria was highest among men; it decreased with increasing year of diabetes onset from 1933 to 1952, and decreased with increasing age at onset. The relative mortality was extremely high among patients with persistent proteinuria, increasing to a maximum of about 100 at age 35 years. Patients not developing proteinuria had a relatively constant low relative mortality of about 2. The decreasing incidence of persistent proteinuria and the decreasing mortality with increasing calendar year of diabetes onset resulted in a 50% increase in life-expectancy among patients diagnosed in 1950 compared with patients diagnosed in 1935. In patients who developed persistent proteinuria, relative mortality was higher in women than men at all ages. In patients who did not develop proteinuria, relative mortality was similar in men and women after the age of 35. Uraemia was the main cause of death in patients with persistent proteinuria, although cardiovascular deaths were more frequent than in patients without proteinuria. Thus, proteinuria is associated not only with death from uraemia but also from cardiovascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Low values of estimated glomerular filtration rate (eGFR) predispose to acute kidney injury, and proteinuria is a marker of kidney disease. We aimed to investigate how eGFR and proteinuria jointly modified the risks of acute kidney injury and subsequent adverse clinical outcomes.
We did a cohort study of 920,985 adults residing in Alberta, Canada, between 2002 and 2007. Participants not needing chronic dialysis at baseline and with at least one outpatient measurement of both serum creatinine concentration and proteinuria (urine dipstick or albumin-creatinine ratio) were included. We assessed hospital admission with acute kidney injury with validated administrative codes; other outcomes were all-cause mortality and a composite renal outcome of end-stage renal disease or doubling of serum creatinine concentration.
During median follow-up of 35 months (range 0-59 months), 6520 (0·7%) participants were admitted with acute kidney injury. In those with eGFR 60 mL/min per 1·73 m(2) or greater, the adjusted risk of admission with this disorder was about 4 times higher in those with heavy proteinuria measured by dipstick (rate ratio 4·4 vs no proteinuria, 95% CI 3·7-5·2). The adjusted rates of admission with acute kidney injury and kidney injury needing dialysis remained high in participants with heavy dipstick proteinuria for all values of eGFR. The adjusted rates of death and the composite renal outcome were also high in participants admitted with acute kidney injury, although the rise associated with this injury was attenuated in those with low baseline eGFR and heavy proteinuria.
These findings suggest that information on proteinuria and eGFR should be used together when identifying people at risk of acute kidney injury, and that an episode of acute kidney injury provides further long-term prognostic information in addition to eGFR and proteinuria.
The study was funded by an interdisciplinary team grant from Alberta Heritage Foundation for Medical Research.
Comment In: Lancet. 2010 Dec 18;376(9758):2046-821094998