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Our study aimed to investigate the effects of iron-deficiency anemia (IDA) on renal tubular functions before and after iron treatment for infants and children with IDA. We measured urinary levels of two kidney injury markers: neutrophil gelatinase-associated lipocalin (NGAL) and liver-type fatty acid-binding protein (L-FABP).Thirty-six infants and children with IDA and 20 matched healthy controls were included. We assessed different laboratory parameters, estimated glomerular filtration rate, urinary levels of NGAL, and L-FABP. Urinary kidney injury markers were measured in IDA patients before and after 3 months of oral iron therapy.IDA patients had significantly higher urinary NGAL and L-FABP levels compared to their healthy controls. After 3 months of oral iron treatment, there was a significant improvement (decrease) in urinary NGAL and L-FABP in infants and children with IDA. Urinary markers returned to normal levels (healthy control levels) in children with IDA, but not for infants with IDA compared to their healthy controls.Subclinical kidney injury was found in infants and children with IDA. This injury was completely reversible in older children with IDA and partially reversible in infants with IDA after iron therapy. Higher urinary levels of kidney injury molecules in IDA infants after iron treatment are suggestive of more sensitivity of these infants to oxidative stress caused by iron therapy or may be due to the immaturity of the kidney and more damage caused by IDA which may require more time to recover.

The time-course of changes in baroreceptor reflex sensitivity during the reversal of Goldblatt two-kidney one-clip hypertension was studied in male Wistar rats. Groups of animals were studied before and 1, 3, 7, 14 and 25 days after removal of a left renal artery clip of 0.18 mm internal diameter. Normotensive rats of comparable ages were included as controls. Baroreflex sensitivity increased from 0.299 +/- 0.072 ms/mmHg (n = 8) in 25 day hypertensive rats to 0.657 +/- 0.155 and 0.786 +/- 0.093 ms/mmHg (n = 8) in 1 day and 3 day declipped animals respectively. Baroreflex sensitivity in the 1 day declipped rats was inversely related to the level of blood pressure. Baroreflex sensitivity is restored early when renovascular hypertension is reversed. This is unlikely to be due solely to regression of structural vascular adaptation.

A "bolus" dose (110 microgram) of the angiotesin II (A II)-blocker 1-Sar-8-Ala-A II (Saralasin, S) followed by its slow rate infusion (5 microgram/min/rat) for thirty min, was injected before and after the complete ganglionic blockade by pentolinium (P) in unanaesthetized unilaterally clipped renal hypertensive rats (the opposite kidney remained untouched). Pentolinium was also injected like a "bolus" dose (3 mg) followed by slow infusion (0.1 mg/min/rat) for thirty min. The observations were made until the fifth week after clipping the left renal artery. A consistent maximal hypotensive response was observed after the "bolus test" with both drugs. When S was the first drug injected, an inverse correlation was found between the percent decrease in arterial pressure (BP) by S and the percent decrease in BP by P (r = --0.83, P0.01, n = 8). Thus whenever a greater hypotensive effect was obtained by S, a smaller neural pressor component remained to be blocked by P. On the other hand, when P was the first drug injected a lesser A II pressor component remained to be blocked by S in the hypertensive rats. The results suggest that a considerable A II pressor effect in two-kidney renovascular hypertension is mediated via neurogenic mechanisms from the first week. A direct pressor vasoconstriction was found to be significant in cases with very high plasma-renin activity.

Chronic systolic blood pressure (SBP) studies were conducted in conscious female rats which received single intraperitoneal injections of 0, 100, 200, 1000, or 2000 micrograms Cd (as acetate). All doses of Cd temporarily increased SBP by 10-15 mm Hg between 3-6 days after treatment. Those rats which had received 100 micrograms Cd were then given four additional doses at 14 day intervals. These injections generally produced similar brief SBP elevation. However, sustained hypertension was not produced in any of the protocols. After Cd exposure, SBP was unaffected by substituting saline as the drinking source, but daily water and saline intake were lower in Cd-treated rats. Cd pretreatment did not affect the incidence of hypertension produced by unilateral renal artery constriction but slightly decreased its severity. Administration of Cd had no effect on rats with chronic two kidney renal hypertension. These results suggest that Cd only transiently increased SBP and did not increase susceptibility for developing experimental hypertension.