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Biomedical subjects

J P Guignard

Publications and source records attributed to J P Guignard.

At least 19 recordsLinked to original sources
PubMed2003

Glomerular filtration rate: measure creatinine and height rather than cystatin C!

AIM: Inulin clearance (Cin) is the gold standard for assessing glomerular filtration rate (GFR). Other methods are based on the plasma creatinine concentration (Pcreat), creatinine clearance (Ccreat), the Haycock-Schwartz formula and the plasma concentration of cystatin C (PcysC), a 13 kDa basic protein produced at a constant rate by all nucleated cells. The present prospective study was thus designed to evaluate the reliability of PcysC as a marker of GFR in comparison with that of Pcreat, Ccreat and the Haycock-Schwartz formula, using Cin as the gold standard. METHODS: Ninety-nine children (51 m/48 f), with a median age of 8.3 y (1.0-17.9) were studied. Using a cut-off for Cin of 100 ml/min per 1.73 m2, 54 children (54.5%) had impaired GFR. Those with normal GFR were comparable for age, height, weight and body mass index. RESULTS: Logistic regression, ROC analysis and linear regression all showed that Ccreat was the best parameter to discriminate between impaired and normal GFR, followed by the Haycock-Schwartz formula, PcysC, and finally Pcreat, each one being significantly more predictive than the next. CONCLUSION: GFR is better assessed by the Haycock-Schwartz formula than by PcysC or Pcreat alone. It is therefore concluded that when urine collection is not possible, simply measuring the child's Pcreat and height is the best, easiest and cheapest way to assess GFR.

Adolescent↗
PubMed2001

The renal hemodynamic effects of Aspirin in newborn and young adult rabbits.

A group of neonatal (n=10) and 12-week-old (n=12) anesthetized, ventilated New Zealand white rabbits received an acute i.v. dose (40 mg/kg body weight) of acetylsalicylic acid (ASA, Aspirin). In the neonatal animals, i.v. ASA caused within 20 min a significant (P<0.01) fall in renal blood flow and glomerular filtration rate (GFR), with an equally significant (P<0.01) increase in filtration fraction and renal vascular resistance. The latter indicates greatly augmented renal vasconstriction or more precisely reduction in intrarenal vasodilatation by inhibition of vasodilatory prostaglandin (PG) synthesis. Urine volume decreased. The 12-week-old young adult animals responded in a similar, but significantly attenuated fashion. These experiments demonstrate that inhibition of PG synthesis in neonatal animals causes very rapid, reversible vasoconstriction, with a reduction in GFR. In addition, this study confirms previous observations that the renal hemodynamic response to the inhibition of PG synthesis is far more pronounced in neonatal animals than in (young) adult rabbits.

Age Factors↗
PubMed2001

Dipstick measurements of urine specific gravity are unreliable.

AIM: To evaluate the reliability of dipstick measurements of urine specific gravity (U-SG). METHODS: Fresh urine specimens were tested for urine pH and osmolality (U-pH, U-Osm) by a pH meter and an osmometer, and for U-SG by three different methods (refractometry, automatic readout of a dipstick (Clinitek-50), and (visual) change of colour of the dipstick). RESULTS: The correlations between the visual U-SG dipstick measurements and U-SG determined by a refractometer and the comparison of Clinitek((R))-50 dipstick U-SG measurements with U-Osm were less than optimal, showing very wide scatter of values. Only the U-SG refractometer values and U-Osm had a good linear correlation. The tested dipstick was unreliable for the bedside determination of U-SG, even after correction for U-pH, as recommended by the manufacturer. CONCLUSIONS: Among the bedside determinations, only refractometry gives reliable U-SG results. Dipstick U-SG measurements should be abandoned.

Humans↗
PubMed2001

[Kinetics of potassium transfer during hemodialysis].

INTRODUCTION: In order to study whether the removal of potassium in haemodialysis patients could be increased, we analyzed the kinetics of potassium transfer in the dialyzer. METHOD: 40 patients were included in the study. We studied: a) in vitro potassium exchanges between erythrocytes and plasma; b) plasma and erythrocyte potassium concentrations at dialyzer input and output; c) potassium transfers into the dialysate, using plasma clearance and direct measurement in the collected dialysate and d) erythrocyte potassium concentrations at the beginning and the end of dialysis. RESULTS: In vitro, there is virtually no potassium transfer between erythrocytes and plasma. In vivo, erythrocyte potassium concentration is not affected by the dialyzer (98.7 +/- 6.4 mmol/l to 97.7 +/- 7.5 mmol/l, p = NS). Potassium transfer levels determined by calculated plasma clearance were similar to values obtained by measuring potassium in dialysate (0.71 +/- 0.10 mmol/min vs 0.68 +/- 0.10 mmol/min, p = NS). These results suggest that erythrocytes do not participate in potassium exchange in the dialyzer. This was confirmed by measured erythrocyte potassium concentrations, which were the same at the beginning and the end of dialysis (104.0 +/- 5.6 mmol/l vs 104.2 +/- 5.0 mmol/l, p = NS).

Adult↗
PubMed2001

[Polyuria, pollakiuria, and nocturia in children: diagnostic and therapeutic approach].

Polyuria is defined as the passage of large volumes of diluted urine secondary to an abnormality of urine concentration. This disorder can result either from deficient secretion of vasopressin (cranial diabetes insipidus), or from renal resistance to vasopressin (nephrogenic diabetes insipidus), primary polydipsia, osmotic diuresis, electrolytic disorders or drugs. Suspicion of impaired renal concentration ability can be confirmed by a fluid deprivation test. The administration of exogenous vasopressin allows to clarify the pathogenetic mechanism. Once the mechanism responsible for polyuria has been clarified it is mandatory to search for underlying causes. Treatment of polyuria should be causal, if its origin is known, and/or symptomatic in order to prevent severe dehydration. Symptomatic treatment of cranial diabetes insipidus consists of administering exogenous vasopressin. Salt restriction associated to a combined administration of hydrochlorothiazide/amiloride or hydrochlorothiazide/indomethacin can reduce urine output by 20 to 50% in case of nephrogenic diabetes insipidus. Pollakiuria is defined as a daytime urinary frequency. It can be isolated or may be a manifestation of lower urinary tract infections, bladder instability, nephrolithiasis or concentrated acidic urines. Detailed history and physical examination represent major clues to diagnostic. Therapy of pollakiuria can be causal or symptomatic using anticholinergic drugs or reeducation in case of bladder instability. Nocturia is characterized by voluntary nocturnal micturitions secondary to conditions inducing impaired renal concentration ability, or to heart failure.

Child↗
PubMed2001

[Hyperaminoaciduria in children].

Hyperaminoaciduria is a major disorder to be considered in the event of growth and mental retardation, convulsion and other unexplained clinical symptoms. This review should enable the general practitioner to determine the conditions necessitating urinary and blood amino acid analyses in order to improve the treatment of children presenting rare pathologies, the prognosis of whom depends on the rapidity of the intervention. The diagnosis and treatment of hereditary and renal hyperaminoaciduria are discussed and a physiological and physiopathological synthesis of the tubular reabsorption of amino acids is presented. The different clinical entities associated with hyperaminoaciduria are then briefly described according to their origin (renal or prerenal).

Child↗
PubMed2001

[Exposure in utero to immunosuppressives].

The number of pregnant women receiving immunosuppressive therapy is increasing. Use of immunosuppressants during pregnancy is indicated for anti-rejection therapy in transplantation patients and treatment of autoimmune diseases. Despite the maternal and fetal risks of these pregnancies, the proportion of surviving infants is improving and the possibility that a pregnancy could occur in these women during their childbearing years should be considered. All immunosuppressant drugs and their metabolites cross the placenta, raising questions about the long-term outcome of the children exposed to these agents in utera. There is no increased risk of congenital anomalies. However, there is an elevated incidence of prematurity, intrauterine growth retardation (IUGR) and therefore low birthweight, as well as maternal hypertension and preeclampsia. The most frequent neonatal complications are those associated with prematurity and IUGR, as well as adrenal insufficiency with corticosteroids, immunological disturbances with azathioprine and cyclosporin, and hyperkalemia with tacrolimus. The long-term follow-up of infants exposed to immunosuppressants in utero is still limited and experimental studies raise the question whether there could be an increased incidence at adult age of some pathologies including renal insufficiency, hypertension and diabetes. The follow-up of these infants should be carefully organized and multidisciplinary, taking the perinatal context into account.

Abnormalities, Drug-Induced↗
PubMed2000

Endothelin, angiotensin II and adenosine in acute cyclosporine A nephrotoxicity.

We previously developed a model of acute cyclosporine A (CsA)-induced vasomotor nephrotoxicity in rabbits. In the present study, we evaluated the role of endothelin (ET), angiotensin II (AII) and adenosine in this experimental model. All animals received CsA (25 mg/kg/day) for 5 days. Renal function parameters were first measured in a 30-min period, showing renal insufficiency in all animals. Then, rabbits were administered bosentan (10 mg/kg; antagonist of ET(AB) receptors), perindopril (20 microg/kg; angiotensin-converting enzyme inhibitor), or theophylline (1 mg/kg; adenosine receptor blocker at micromolar concentrations). After a 40-min equilibration period, renal function was assessed again for 30 min. Bosentan, perindopril and theophylline significantly reduced renal vascular resistance (-28+/-5%, -39+/-7% and -8+/-3%, respectively), and improved renal blood flow (+38+/-15%, +66+/-16% and +20+/-5%), glomerular filtration rate (+33+/-9%, +52+/-13% and +50+/-8%) and diuresis (+48+/-9%, +76+/-19% and +73+/-14%). Filtration fraction was unchanged with bosentan, decreased with perindopril (-10+/-9%) and increased with theophylline (+24+/-5%). The overall results suggest that ET, AII and adenosine are involved in the acute renal failure induced by CsA. We conclude that CsA administration for 5 days induced a vasomotor nephropathy with ET- and adenosine-mediated afferent arteriolar constriction as well as ET- and AII-mediated efferent arteriolar constriction.

Acute Disease↗
PubMed2000

The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy.

The healthy term, and particularly the premature infant, is born with a very low glomerular filtration rate (GFR), controlled by a delicate balance of intrarenal vasoconstrictor and vasodilator forces. Vasoactive disturbances can easily further reduce the already low GFR. The newborn infant is thus prone to develop vasomotor nephropathy (VMNP) or acute renal failure (ARF). The main causes for ARF at this young age are prerenal mechanisms, and include hypotension, hypovolemia, hypoxemia perinatal asphyxia, and neonatal septicemia. Other causes include the administration of angiotensin converting enzyme inhibitors, indomethacin and tolazoline. The most-important factors governing the ultimate renal prognosis are the severity of the underlying disorder, the rapidity of an accurate diagnosis, prompt treatment, and avoidance of severe iatrogenic complications. The immediate treatment is of particular importance in VMNP, i.e., prerenal ischemic ARF, and consists of correcting abnormalities in fluid homeostasis and reduction of the complications of the acute azotemic state (uremia, hyperkalemia, acidosis, and hypertension). In severe and prolonged (established) ARF, temporary dialysis therapy may be indicated. Prerenal ARF with oliguria or anuria warrants immediate volume resuscitation. Special attention should be given to infants with congestive heart failure (CHF). The sick neonate with persistent oliguria and CHF should be treated with intravenous dopamine. Furosemide (FM) is the second line of therapy for babies with indomethacin-induced ARF. In most other conditions, the therapeutic effect of FM is limited to a transient increase in urine flow, without improving basic renal function. The special conditions of the maturing kidney have to be appreciated in order to protect babies from undue renal injury. With the increasing knowledge of the mechanisms governing the development of ARF, progress has been made in the development of new treatment modalities. For example theophylline, calcium antagonists, ATP-MgCl2, thyroxine, and a variety of cytokines may in the near future be used to prevent or ameliorate VMNP and/or recently established ARF. With a combination of time-honored and new therapeutic strategies, there may well be a brighter future for neonates with vasomotor, prerenal, ischemic ARF.

Humans↗
PubMed2000

Management of acute renal failure in newborns.

Acute renal failure (ARF) is a frequent clinical condition in neonatal intensive care units. Plasma creatinine concentrations should be used with some caution for ARF diagnosis in the first days of life. An intravenous fluid challenge allows differentiation of prerenal failure and intrinsic renal failure. All clinical conditions associated with hypovolemia, hypoxemia, and hypotension in the newborn infant may lead to renal insufficiency, the leading causes being perinatal anoxia-ischemia and sepsis. The initial treatment mainly relies on correction of hypotension, acidosis, and hypoxemia, in order to reduce renal vasoconstriction and improve renal perfusion. If necessary, the main renal replacement therapy is usually peritoneal dialysis even if skilled medical and nursing personnel are available in some neonatal intensive care units to perform hemofiltration and hemodiafiltration safely.

Acute Kidney Injury↗
PubMed2000

Acute cyclosporine A-induced nephrotoxicity: a rabbit model.

Chronic cyclosporine A (CsA) nephrotoxicity has been widely assessed but only few studies have described acute nephrotoxicity. As CsA is now used for short periods, we developed an experimental model of acute CsA-induced nephrotoxicity. Renal clearances of inulin and para-aminohippurate were assessed in 35 New Zealand rabbits. Group 1: control, no treatment; group 2: CsA 25 mg/kg per day in 0.5 ml/kg per day for 5 days; group 3: vehicle Cremophor-EL, 0.5 ml/kg per day for 5 days; group 4: follow-up, the same as group 2, then CsA discontinuation for 31 days. Compared with group 1, CsA significantly decreased glomerular filtration rate (GFR), renal blood flow (RBF), and diuresis, with a significant increase in renal vascular resistance (RVR). The proportional fall in GFR (-32.3%) and RBF (-33.1%) suggests both pre- and postglomerular vasoconstriction. Discontinuation of CsA in group 4 led to normalization of RVR with improvement of other renal function parameters. Compared with group 1, Cremophor-EL induced no significant changes but an increased RBF. Microvacuolization of proximal tubule epithelial cells was the sole histological abnormality observed only in group 2. The overall results suggest that CsA induced a vasomotor acute renal failure which was not due to Cremophor-EL. This effect was partly reversible after discontinuation of treatment.

Acute Disease↗