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1	Iohexol et fonction rénale en réanimation : contribution diagnostique et toxicité / Iohexol and kidney function in intensive care unit : contribution for diagnosis and toxicity Salmon Gandonniere, Charlotte 10 December 2018 (has links) En réanimation, il n’existe pas de gold standard pour estimer le débit de filtration glomérulaire (DFG). Nous avons mesuré la clairance du iohexol chez 20 patients en insuffisance circulatoire aiguë (injection de 5 mL de iohexol et cinétique riche sur 24h). Les clairances urinaire et plasmatique étaient équivalentes ; la clairance plasmatique n’était pas influencée par le remplissage. Nous avons étudié la distribution de la clairance du iohexol chez 85 patients en insuffisance circulatoire aiguë. Quarante-et-un patients (48%) avaient un DFG < 30 mL.min-1, 29 (34%) entre 30 et 60mL.min-1, 10 (12%) entre 60 et 90mL.min-1, 4 (5%) entre 90 et 130 mL.min-1 et 1 (1%) > 130 mL.min-1. Nous avons mesuré les biomarqueurs lésionnels [TIMP-2].[IGFBP-7] juste avant, 6h et 24 h après un scanner injecté en réanimation; il n’y a pas eu d’augmentation significative des biomarqueurs, confortant l’hypothèse d’une toxicité négligeable des produits de contraste iodés en réanimation. En conclusion, le iohexol peut être considéré comme un gold standard pour l’estimation du DFG chez des patients en insuffisance circulatoire aiguë en termes de faisabilité, fiabilité et sécurité. / There is no gold standard for glomerular filtration rate (GFR) estimation in intensive care unit. We measured iohexol clearance in 20 patients experiencing acute circulatory failure (5 mL iohexol bolus, urine and blood-sample collections over 24h). Urinary and plasma clearances were equivalent; rapid fluid infusion did not influence plasma clearance. We studied iohexol clearance repartition in 85 patients experiencing acute circulatory failure. Forty-one (48%) had a GFR < 30 mL.min-1, 29 (34%) between 30 and 60mL.min-1, 10 (12%) between 60 and 90mL.min-1, 4 (5%) between 90 and 130 mL.min-1 and 1 (1%) > 130 mL.min-1. We measured lesion biomarkers [TIMP-2].[IGFBP-7], before, 6h and 24h after an injected computed tomography scan; there was no significant raise in the biomarkers. This result supports the hypothesis that contrast media are armless in intensive care units. To conclude, iohexol can be considered as a gold standard for GFR estimation in acute-circulatory-failure patients regarding feasibility, reliability and safety. Débit de filtration glomérulaire Iohexol Réanimation Insuffisance circulatoire aiguë Insuffisance rénale aiguë Hyperfiltration glomérulaire Glomerular filtration rate Iohexol Intensive care unit Acute circulatory failure Acute kidney injury Glomerular hyperfiltration
2	L’impact de la prématurité sur la fonction rénale à l'âge adulte Aeschimann, Claire Simada 07 1900 (has links) La naissance très prématurée (<29 semaines de gestation) affecte environ 10% de la population canadienne chaque année, et la plupart de ces individus survivent jusqu'à l'âge adulte. La prématurité a un impact sur le développement de plusieurs organes, notamment les reins. Les études ont démontré que les adultes nés prématurément, comparativement à ceux nés à terme, présentent un nombre réduit de néphrons et une architecture glomérulaire altérée. Des études épidémiologiques ont également confirmé le risque augmenté de maladie rénale chronique chez les individus nés prématurément. Par ailleurs, les individus nés prématurément ont une pression artérielle plus élevée. Les mécanismes sous-jacents à l'hypertension artérielle consécutive à une naissance prématurée sont encore en cours d'élucidation; il est donc important de comprendre la contribution potentielle des reins. Les conséquences à long terme de la naissance prématurée sur la fonction rénale restent encore insuffisamment étudiées. Avec un capital néphronique réduit, afin de maintenir un débit de filtration glomérulaire (DFG) adéquat, nous postulons que l'une des premières manifestations de la dysfonction rénale chez les adultes nés prématurément serait une hyperfiltration glomérulaire au niveau du néphron individuel (mononéphron). L’hyperfiltration glomérulaire mononéphron pourrait ainsi perpétuer les dommages rénaux et mener plus tardivement à la baisse du DFG. Cette étude observationnelle vise à comparer le débit de filtration glomérulaire (DFG) de 78 jeunes adultes nés prématurément et 78 témoins nés à terme âgés de 18 à 40 ans. Le DFG a été mesuré par scintigraphie rénale au DMSA marqué au technétium 99 (99mTc-DMSA). Nous avons estimé le DFG mononéphron en divisant le DFG par le volume rénal obtenu par échographie. Les résultats ont révélé une réduction du DFG total. Ces différences étaient principalement constatées chez les hommes prématurés versus terme. Nous n’avons pas identifié de différence entre les deux groupes pour les valeurs de DFG mononéphron. Un plus grand volume rénal était associé à un plus grand DFGm tant chez les individus nés prématurément que ceux nés à terme. Il n’y avait pas de corrélation entre le DFGm et les valeurs de tension artérielle ou d’albuminurie. En conclusion, nous notons une diminution du DFG total chez les hommes nés prématurément versus ceux nés à terme. Ceci souligne l’importance d’évaluer la santé rénale à la suite d’une naissance prématurée. / Very preterm birth (<29 weeks of gestation) affects about 10% of the Canadian population each year, and most of these individuals survive into adulthood. Prematurity impacts the development of several organs, including the kidneys. Studies have shown that adults born prematurely, compared to those born at term, have a reduced number of nephrons and altered glomerular architecture. Epidemiological studies have also confirmed the increased risk of chronic kidney disease in individuals born prematurely. Additionally, individuals born prematurely have higher blood pressure. The underlying mechanisms of hypertension following preterm birth are still being elucidated, making it important to understand the potential contribution of the kidneys. The long-term consequences of preterm birth on renal function remain insufficiently studied. With a reduced nephron endowment, to maintain an adequate glomerular filtration rate (GFR), we hypothesize that one of the first manifestations of renal dysfunction in adults born prematurely would be glomerular hyperfiltration at the individual nephron (single-nephron) level. Single-nephron glomerular hyperfiltration could thus perpetuate kidney damage and later lead to a decline in GFR. This observational study aims to compare the glomerular filtration rate (GFR) of 78 young adults born prematurely and 78 term-born controls aged 18 to 40 years. GFR was measured using renal scintigraphy with technetium-99m-labeled DMSA (99mTc-DMSA). We estimated single-nephron GFR by dividing the GFR by the renal volume obtained via ultrasound. The results revealed a reduction in total GFR, but no difference in the estimate of single-nephron GFR in adults born prematurely compared to those born at term. This was predominantly observed when comparing males born preterm versus males born at term. Increased kidney size was associated with increased GFR. There was no correlation between GFR and blood pressure or albuminuria values. In conclusion, at 18-40 years, very preterm birth is associated with an overall decrease in total GFR in males. This underscores the importance of assessing renal health following preterm birth. naissance prématurée cortex rénal fonction glomérulaire échographie volume rénal néphrogénèse albuminurie hyperfiltration glomérulaire premature birth renal cortex glomerular function ultrasound renal volume nephrogenesis albuminuria glomerular hyperfiltration Medicine / Médecine (UMI : 0564)
3	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa Al Salmi Unknown Date (has links) The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study
4	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa Al Salmi Unknown Date (has links) The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study
5	BIRTHWEIGHT AND SUSCEPTIBILITY TO CHRONIC DISEASE Issa Al Salmi Unknown Date (has links) The thesis examines the relationship of birthweight to risk factors and markers, such as proteinuria and glomerular filtration rate, for chronic disease in postnatal life. It made use of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). The AusDiab study is a cross sectional study where baseline data on 11,247 participants were collected in 1999-2000. Participants were recruited from a stratified sample of Australians aged ≥ 25 years, residing in 42 randomly selected urban and non-urban areas (Census Collector Districts) of the six states of Australia and the Northern Territory. The AusDiab study collected an enormous amount of clinical and laboratory data. During the 2004-05 follow-up AusDiab survey, questions about birthweight were included. Participants were asked to state their birthweight, the likely accuracy of the stated birthweight and the source of their stated birthweight. Four hundred and twelve chronic kidney disease (CKD) patients were approached, and 339 agreed to participate in the study. The patients completed the same questionnaire. Medical records were reviewed to check the diagnoses, causes of kidney trouble and SCr levels. Two control subjects, matched for gender and age, were selected for each CKD patient from participants in the AusDiab study who reported their birthweight. Among 7,157 AusDiab participants who responded to the questionnaire, 4,502 reported their birthweights, with a mean (standard deviation) of 3.4 (0.7) kg. The benefit and disadvantages of these data are discussed in chapter three. The data were analysed for the relationship between birthweight and adult body size and composition, disorders of glucose regulation, blood pressure, lipid abnormalities, cardiovascular diseases and glomerular filtration rate. Low birthweight was associated with smaller body build and lower lean mass and total body water in both females and males. In addition low birthweight was associated with central obesity and higher body fat percentage in females, even after taking into account current physical activity and socioeconomic status. Fasting plasma glucose, post load glucose and glycosylated haemoglobin were strongly and inversely correlated with birthweight. In those with low birthweight (< 2.5 kg), the risks for having impaired fasting glucose, impaired glucose tolerance, diabetes and all abnormalities combined were increased by 1.75, 2.22, 2.76 and 2.28 for females and by 1.40, 1.32, 1.98 and 1.49 for males compared to those with normal birthweight (≥ 2.5 kg), respectively. Low birthweight individuals were at higher risk for having high blood pressure ≥ 140/90 mmHg and ≥ 130/85 mmHg compared to those with normal birthweight. People with low birthweight showed a trend towards increased risk for high cholesterol (≥ 5.5 mmol/l) compared to those of normal birthweight. Females with low birthweight had increased risk for high low density lipoprotein cholesterol (≥ 3.5 mmol/l) and triglyceride levels (≥ 1.7 mmol/l) when compared to those with normal birthweight. Males with low birthweight exhibited increased risk for low levels of high density lipoprotein cholesterol (<0.9 mmol/l) than those with normal birthweight. Females with low birthweight were at least 1.39, 1.40, 2.30 and 1.47 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases respectively, compared to those ≥ 2.5 kg. Similarly, males with low birthweight were 1.76, 1.48, 3.34 and 1.70 times more likely to have angina, coronary artery disease, stroke and overall cardiovascular diseases compared to those ≥ 2.5 kg, respectively. The estimated glomerular filtration rate was strongly and positively associated with birthweight, with a predicted increase of 2.6 ml/min (CI 2.1, 3.2) and 3.8 (3.0, 4.5) for each kg of birthweight for females and males, respectively. The odd ratio (95% confidence interval) for low glomerular filtration rate (<61.0 ml/min for female and < 87.4 male) in people of low birthweight compared with those of normal birthweight was 2.04 (1.45, 2.88) for female and 3.4 (2.11, 5.36) for male. One hundred and eighty-nineCKD patients reported their birthweight; 106 were male. Their age was 60.3(15) years. Their birthweight was 3.27 (0.62) kg, vs 3.46 (0.6) kg for their AusDiab controls, p<0.001 and the proportions with birthweight<2.5 kg were 12.17% and 4.44%, p<0.001. Among CKD patients, 22.8%, 21.7%, 18% and 37.6% were in CKD stages 2, 3, 4 and 5 respectively. Birthweights by CKD stage and their AusDiab controls were as follows: 3.38 (0.52) vs 3.49 (0.52), p=0.251 for CKD2; 3.28 (0.54) vs 3.44 (0.54), p=0.121 for CKD3; 3.19 (0.72) vs 3.43 (0.56), p= 0.112 for CKD4 and 3.09 (0.65) vs 3.47 (0.67), p<0.001 for CKD5. The results demonstrate that in an affluent Western country with a good adult health profile, low birthweight people were predisposed to higher rates of glycaemic dysregulation, high blood pressure, dyslipidaemia, cardiovascular diseases and lower glomerular filtration rate in adult life. In all instances it would be prudent to adopt policies of intensified whole of life surveillance of lower birthweight people, anticipating this risk. The general public awareness of the effect of low birthweight on development of chronic diseases in later life is of vital importance. The general public, in addition to the awareness of people in medical practice of the role of low birthweight, will lead to a better management of this group of our population that is increasingly surviving into adulthood. birth weight birthweight birth weight and renal volume BIRTH WEIGHT QUESTIONNAIRE chronic disease Barker Hypothesis Foetal development DOHaD gestational age Anthropometric Characteristics body composition Height weight body mass index Waist Circumference hip circumference Waist-hip Ratio obesity Central Obesity Fatness Lean Body Mass Lean Mass Fat Mass body fat mass Body Fat Percentage body fatness Body Surface Area diabetes Fasting Glucose fasting insulin level glucose tolerance Impaired Fasting Glucose Impaired Glucose Tolerance Glycosylated Hemoglobin HbA1c IFG glucose control glycaemic control Metabolic Syndrome Syndrome X blood pressure Systolic Blood-pressure Diastolic Blood-pressure Systolic Hypertension high blood pressure Hypertension Dyslipidaemia Dyslipidemia Total Cholesterol Triglyceride Low Density Lipoprotein Cholesterol Ldl Cholesterol High Density Lipoprotein Hdl Cholesterol Fibrinogen angina Angina-pectoris Stroke coronary artery disease cardiovascular disease Framingham Framingham Heart Study Framingham Score coronary heart disease Glomerular Filtration glomerular filtration rate Glomerular Hyperfiltration Glomerular Injury Glomerular Number Nephrogenesis Nephron Endowment Nephron Number NKF-K/DQQI Classification Chronic Kidney Disease (ckd) Chronic Kidney Failure Kidney Failure CKD STAGES end-stage renal disease (ESRD) end-stage renal failure Cockcroft-gault MDRD formula Serum Creatinine Urinary Creatinine albuminuria Albuminuria:creatinine Ratio Kidney Development Kidney dysfunction low birth weight low birth weight Pre-term Birth AusDiab Study case control longitudinal observational study

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