Appropriate use of quality measures: Response to “risk factors for hospital readmission within 30 days: A new quality measure for children with sickle cell disease”

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/64337/1/22212_ftp.pd

Invited Review Recognition and management of angiotensin converting enzyme inhibitor fetopathy

Angiotensin converting enzyme (ACE) inhibitors are extensively used for the treatment of hypertension, to decrease proteinuria, and to mitigate hyperfiltration. These drugs now have been shown to be fetotoxic causing profound fetal hypotension, renal tubular dysplasia, anuria-oligohydramnios, growth restriction, hypocalvaria, and death when used in the second and third trimesters of pregnancy. We recommend that ACE inhibitors not be used in pregnancy. However, if a child is born with ACE inhibitor fetopathy, aggressive therapy with dialysis to remove the inhibitor may mitigate the profound hypotensive effects. Therapy will depend on the specific ACE inhibitor, and care recommendations cannot be generalized for the entire class of drugs as their protein binding and volume of distribution differ substantially.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47835/1/467_2005_Article_BF02254221.pd

Renal tubular dysgenesis in twins

In a fetal autopsy series, we have explored the occurrence of renal tubular dysgenesis in twins. Renal tubular dysgenesis was found exclusively among those monozygotic twins with evidence of twin transfusion syndrome, particularly in those donor twins with oligohydramnios and growth restriction. We infer that hypotension in the donor twin of the twin transfusion syndrome pair is responsible for the failure of proximal convoluted tubule differentiation, and the disturbance of renal function is manifested as oligohydramnios prenatally, and either oliguria or tubular dysfunction postnatally.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42296/1/467-12-5-408_80120408.pd

Ask the expert

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47830/1/467_2004_Article_BF00862507.pd

“Dilatation” of the left renal vein on computed tomography in children: A normal variant

Compression of the left renal vein (LRV) between the superior mesenteric artery and the aorta is thought to be a cause of hematuria, periureteral and gonadal varices, and varicocele (“Nutcracker phenomenon”). Previous investigators have suggested that this diagnosis can be made on computed tomography when the LRV ratio ≥1.5 (the diameter of the LRV proximal to the aorto-mesenteric angle divided by the diameter of the LRV distal to the aorto-mesenteric angle). This study was designed to establish the normal range for the LRV ratio on CT in children. The LRV ratio was measured in thirty-nine consecutive children undergoing intravenously enhanced CT of the abdomen. None of the children had hematuria on urinalysis immediately before or after the CT. Children with any known abnormality involving the kidneys, adrenal glands, IVC, or renal or gonadal veins were excluded. The patients ranged in age from 3.4 to 18.5 years (mean=10.6 years). LRV ratio ranged from 0.78 to 2.00 (mean=1.46; S.D.=0.312). Twenty of the 39 children (51.3%) had a LRV ratio ≥1.50. The conclusion is that the normal range for the LRV ration is too wide for it to be useful in diagnosing LRV entrapment and that a LRV ratio ≥1.5 on CT is normal in children.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46695/1/247_2005_Article_BF02018620.pd

Radiographic manifestations of experimental aluminum toxicity in growing bone

To evaluate the effect of aluminum on growing bone in the presence of normal renal function, the following experiment was performed. Eight littermate pair-fed pigs (5 weeks old) were randomly assigned to one of two study groups: control C, n =4, or aluminum treated Al, n =4. Daily intravenous injections of either aluminum 1.5 mg/kg/day (Al group) or vehicle only (C group) were given during the 8-week duration of the study. The radiographic findings which appeared in the aluminum-treated group and not in the controls consisted of areas of sclerosis in the submetaphyseal regions and the periphery of epiphyses. In addition there was separation of the anterior tibial tubercle. The growth plates did not increase in width despite the presence of osteomalacia and histologic evidence of extensive deposition of aluminum in bone. The area of sclerosis visualized in the radiographs correlated histologically with thickened bony trabeculae. The increased width of these trabeculae is attributable to an increase in primary spongiosum and broadened seams of osteoid.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46782/1/256_2004_Article_BF00356955.pd

Neoral induction in pediatric renal transplantation

Neoral was instituted in pediatric renal transplant patients with the hypothesis it would have more predictable kinetics than Sandimmun. However, significant questions have arisen concerning potential toxicity and dosing interval related to its rapid absorption with subsequent high initial peak. This is compounded by the fact that children appear to metabolize cyclosporine at a greater rate than adults. This combination of a rapid peak and rapid absorption may then result in lower trough levels at 12 h. We compared the trough cyclosporine levels of nine children who received Neoral with nine who received Sandimmun at the time of initial transplantation. More frequent dosing (every 8 h) was required in the Neoral population compared with the Sandimmun population for the 1st month in order to obtain comparable trough levels. Beyond the initial 4–6 weeks, trough levels were similar for Neoral and Sandimmun. Whereas 1-month creatinine levels and blood pressures were similar, the number of blood pressure medications was significantly higher in the Neoral group. At 5.5 ± 1.1 months’ followup, a single patient in the current Neoral group and in the retrospective Sandimmun group each experienced a single OKT3 allograft-treated rejection. We suggest that the area under the curve is different in Neoral than Sandimmun, and the initial dosing frequency may need to be adjusted accordingly.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42295/1/467-12-1-2_80120002.pd

Hepatic Abnormalities Associated with Aluminum Loading in Piglets

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141476/1/jpen0293.pd

Aluminum toxicity in childhood

Aluminum intoxication is an iatrogenic disease caused by the use of aluminum compounds for phosphate binding and by the contamination of parenteral fluids. Although organ aluminum deposition was noted as early as 1880 and toxicity was documented in the 1960s, the inability to accurately measure serum and tissue aluminum prevented delineation of its toxic effects until the 1970s. Aluminum toxicity has now been conclusively shown to cause encephalopathy, metabolic bone disease, and microcytic anemia.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47831/1/467_2004_Article_BF00869743.pd

Aluminum loading in children with chronic renal failure

Aluminum loading in children with chronic renal failure. Plasma aluminum levels were measured in 17 children with chronic renal failure who were receiving aluminum containing antacids for the control of hyperphosphatemia. Seven children were on hemodialysis, five on peritoneal dialysis, and five were awaiting dialysis with creatinine clearances between 10 to 20 cc/min/1.73m2. Plasma aluminum levels correlated directly with oral aluminum dosage; extremely high levels were documented in small, nondialyzed children. Bone aluminum levels were measured in four children with high plasma levels and confirmed significant aluminum loading. Other factors such as the level of aluminum in dialysate and tap water were measured and were not contributory. All patients with plasma aluminum levels greater than 100 µg/liter had signs of aluminum toxicity and were receiving greater than 75 mg/kg/day of elemental aluminum orally. We concluded that children who require greater than 30 mg/kg/day of elemental aluminum to control hyperphosphatemia should have plasma aluminum levels monitored and/or be considered for other forms of therapy including more restricted diets and earlier or more aggressive dialysis.Surcharge aluminique chez des enfants en insuffisance rénale chronique. Les concentrations plasmatiques d'aluminium ont été déterminées chez 17 enfants en insuffisance rénale chronique recevant des antiacides contenant de l'aluminium pour contrôler leur hyperphosphatémie. Sept enfants étaient en hémodialyse, cinq en dialyse péritonéale et cinq étaient en attente de dialyse avec des clearances de la créatinine entre 10 à 20 cc/min/1.73 m2. Les niveaux plasmatiques d'aluminium étaient directement corrélés à la dose orale d'aluminium; des niveaux extrêmement élevés ont été documentés chez de petits enfants non dialysés. Les niveaux d'aluminium osseux ont été mesurés chez quatre enfants avec des niveaux plasmatiques élevés et confirmant une surcharge aluminique significative. D'autres facteurs comme le niveau d'aluminium dans le dialysat et l'eau du robinet ont été mesurés mais n'étaient pas contributifs. Tous les malades dont l'aluminium plasmatique dépassait 100 µg/litre avaient des signes de toxicité aluminique et recevaient >75 mg/kg/jour d'aluminium-élément oralement. Nous avons conclu que les enfants nécessitant >30 mg/kg/jour d'aluminium-élément pour contrôler leur hyperphosphatémie devraient avoir leur niveau plasmatique d'aluminium surveillé, et/ou devraient être candidats à d'autres formes de traitement notamment des régimes plus restreints et une dialyse plus précoce ou plus agressive