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J L Pimentel

Publications and source records attributed to J L Pimentel.

12 recordsLinked to original sources

Low anion gap.

BACKGROUND: The purpose of this review is to provide a differential diagnosis for a low anion gap. METHODS: We describe the anatomy of the anion gap. Also, we follow-up with a review of the English-language literature describing the causes of a low anion gap. During the past 15 years, the introduction and widespread clinical use of ion-selective electrode methodology for measuring serum electrolyte values has caused a major fall in the normal range of the anion gap from 12 mEq/L +/- 4 mEq/L to 6 mEq/L +/- 3 mEq/L; therefore, a new definition for a low anion gap is in order. RESULTS: Based on current clinical data, an anion gap value of < 3 mEq/L should be considered low. A low anion gap is a useful diagnostic tool, but its clinical significance is often unrecognized. Also, it may be a handy clinical clue for the diagnosis of life-threatening intoxications or occult neoplasms, such as multiple myeloma. The baseline low anion gap may mask the identification of a high gap metabolic acidosis in certain patients. CONCLUSIONS: Interpretation of a low anion gap can provide valuable clinical information.

Acid-Base Equilibrium↗

Role of angiotensin II in the expression and regulation of transforming growth factor-beta in obstructive nephropathy.

Unilateral ureteral obstruction (UUO) leads to fibrosis of the obstructed kidney. We tested the hypothesis that interstitial fibrosis in UUO results, at least in part, from enhanced expression of transforming growth factor-beta (TGF-beta) which in turn is regulated by local angiotensin II (Ang II) generation. (The generic name TGF-beta is used to discuss properties shared by all isoforms, but special reference to other isoforms is made when specifically needed.) Using Northern blot and immunohistochemical analysis, we examined the expression of TGF-beta in rat kidneys after 24 hours (aUUO) and one week (cUUO) of obstruction. Obstructed kidneys from both periods had increased interstitial and perivascular TGF-beta immunoreactivity compared to contralateral and sham kidneys, in which immunostaining was confined to the inner medulla. Relative abundance of all TGF-beta mRNA isoforms were higher in the obstructed than in contralateral and sham kidneys in both aUUO and cUUO. Expression of TGF-beta isoforms varied according to site (cortex vs. medulla), segment of the nephron, type of cells and duration of the obstruction. The increase in TGF-beta immunoreactivity and mRNA levels in aUUO and cUUO was almost totally abolished by pretreatment with losartan. We conclude that in UUO: (a) TGF-beta gene expression is increased and differentially regulated; (b) Ang II, at least partially, mediates the overexpression of TGF-beta gene; and (c) Ang II may play a central role in fibrogenesis in this and other models of tubulointerstitial disease.

Angiotensin II↗

Sequential changes in renal expression of renin-angiotensin system genes in acute unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) alters the expression of genes encoding for the renin-angiotensin system (RAS). We tested the hypothesis that changes in RAS genes expression occur soon after obstruction. Indeed, measurements during the first 24 hours of UUO showed up-regulation of renin mRNA in the obstructed kidney at 1 hour. UUO also led to increases in PRA and renal renin content, ACE activity and Ang II concentration in the experimental kidney. The obstructed kidney relative abundance of renin mRNA was increased compared to basal at 1, 2, 6, and 24 hours; the contralateral kidney renin mRNA expression was reduced. AT1-R mRNA expression was diminished at 6 and 24 hours in the obstructed kidney compared to contralateral and sham kidneys. ACE activity was up-regulated in the obstructed kidney and transiently down-regulated in the contralateral kidney. These findings show for the first time that activation of the RAS results from as little as 1 hour of UUO and that up-regulation of renin mRNA and ACE activity lead to increase Ang II production which down-regulates AT1-R mRNA as early as 6 hours post-UUO. These studies establish a pattern of sequential, differential regulation of the RAS genes in acute UUO that provide an explanation for the hemodynamic changes in this condition.

Acetylcholinesterase↗

Regulation of the renal angiotensin II receptor gene in acute unilateral ureteral obstruction.

We have shown that acute (24-hr) unilateral ureteral obstruction (UUO) induces the genes encoding for renin, in juxtaglomerular apparatuses and in tubules, for angiotensin converting enzyme in vascular endothelial cells, and for angiotensinogen in perivascular fat. These molecular changes occur in temporal association to marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR), suggesting that angiotensin II (Ang II) is at least partly responsible for the renal vasoconstriction. We tested the hypothesis that down-regulation of the Ang II type-1 receptor (AT1-R) gene occurs in UUO in response to Ang II, by examining the effects of an ACE inhibitor [lisinopril (Li), 5 mg/kg/day] and of the specific nonpeptidic AT1-R blocker, losartan (Lo) (10 mg/kg/day). UUO or sham operated (which included manipulation but not obstruction of the ureter) rats (S) were studied. Northern blot analysis of the steady state concentration of AT1-R mRNA corrected for GAPDH mRNA showed a marked decrease in receptor expression (-77%, N = 4, P < 0.01) in the obstructed kidney (UUO) compared to S; sham diminished gene expression modestly compared to the contralateral kidneys (C) of UUO. In situ hybridization for AT1-R mRNA also showed diminished expression in UUO compared to C kidneys (N = 4). Treatment of UUO rats (N = 4) with Lo increased AT1-R mRNA five times above the levels in UUO rats receiving vehicle; the increase induced by Li was 50% that of Lo; S (N = 4) and C (N = 4) did not change. Losartan, but not vehicle treatment increased RBF (sixfold) and GFR (fivefold) in the UUO kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Unexpected encephalopathy in chronic renal failure: hyperammonemia complicating acute peritonitis.

A woman with mild chronic renal insufficiency was being treated with glucocorticoids for a presumed chronic inflammatory disease. She developed peritonitis arising from a pelvic abscess, which was drained without complications. Unexpectedly, she became obtunded, and eventually, the neurologic dysfunction was linked to hyperammonemia in spite of normal liver function tests. Hyperammonemia was only transiently controlled in spite of protein restriction, repeated hemodialysis, and the use of biochemical means to reduce ammonia. A recurrent pelvic abscess was drained, and hyperammonemia disappeared. A review of ammonia and nitrogen metabolism indicates that bypassing the liver with shunting of ammonia into the systemic circulation should be added to the causes of symptomatic hyperammonemia. Treatment requires the elimination of the bacteria.

Abscess↗

Regulation of renin-angiotensin system in unilateral ureteral obstruction.

The effect of 24-hour unilateral ureteral obstruction (UUO) on the expression and regulation of the renin-angiotensin system (RAS) in rats and of pretreatment with lisinopril (5 mg/kg/day) or the AT1-R inhibitor, losartan, (10 mg/kg/day) on renal hemodynamics was evaluated. Both drugs improved the post-obstructed kidney (POK) renal hemodynamics, lowered MAP, and normalized eicosanoid excretion by the POK. Cortex and medulla POK:CK ratio of relative density R mRNA was approximately 3.5 for both. Sham, POK, and CK showed renin immunoreactivity and R mRNA exclusively in juxtaglomerular position. In addition, in POK renin was expressed in mesangial cells, along greater lengths of afferent arterioles and in dilated distal tubules and loops of Henle. In situ hybridization revealed that approximately 20% more glomeruli in POK than CK overexpressed R mRNA. Blood vessels of POK consistently showed greater ACE and Ao mRNA expression than CK. Overexpression of the genes coding for members of the RAS is possibly responsible for local Ang II production which, in view of the response to CEI and AT1-R inhibitors, is at least partly responsible for the severe hemodynamic changes in UUO.

Animals↗

Immune response of chicks fed various levels of zinc.

Five experiments were conducted to determine the effects of zinc intake on the immune response of chicks. Ancona chicks (Experiment 1), New Hampshire (Experiment 2), New Hampshire x Leghorn (Experiment 3), and broiler chicks (Experiments 4 and 5) were fed semipurified (Experiments 1, 2, 3, and 4) or corn and soybean meal diets (Experiment 5) containing from 8 to 88 micrograms zinc/g of diet. An extra group of chicks in Experiments 1, 2, and 4 were fed a diet adequate in zinc but at an intake similar to that of chicks fed the lowest zinc level in each respective experiment. Low zinc intake (less that 28 micrograms zinc/g of diet) suppressed body weight at all times measured. The effect of zinc intake on the size of lymphoid tissues was variable, but at 5 wk of age, chicks fed 8 micrograms zinc/g of diet had smaller bursae of Fabricius and thymi than those fed additional zinc. Zinc intake had no influence on the primary and secondary immune response to SRBC or delayed hypersensitivity to phytohemagglutinin-P (PHA) or human gamma globulin in Ancona and broiler chicks. However, zinc intake did have a small effect in chicks from the New Hampshire parents. In Experiments 1, 2, and 4 (at least at certain times), antibody titers were reduced in pair-fed chicks. Thus, although zinc supplementation at the levels of practical diets did not affect immune function, feed restriction did.

Animals↗

Research note: increased growth of chicks and poults obtained from hens injected with jackbean urease.

Two experiments were conducted using 120 Single Comb White Leghorn (SCWL) hens and 40 turkey hens. Hens were randomly assigned to two treatments: those injected with urease and controls injected only with adjuvant. At 22 wk of age, half of the SCWL hens were injected intramuscularly with 12 Sumner units of jackbean urease suspended in incomplete adjuvant six times in 26 wk. Turkey hens were injected twice at weekly intervals with 70 Sumner units. The other half of the breeders received adjuvant without urease (control). Urease injection into SCWL hens had no effect on feed consumption, feed conversion, and percentage fertility, hatchability, and hatch of all eggs set, but egg weight and body weight of chicks at hatch and at 3 wk of age were significantly higher as compared with the control hens. In the case of turkey hens, percentage hatchability and progeny body weight were significantly higher as a result of urease injection.

Animals↗

Water consumption and fecal moisture of laying hens fed wheat middlings and corn-soybean-alfalfa meal diets.

Hens, housed on the floor and fed a diet containing 89% wheat middlings (WM) either as mash or pellets, consumed more feed and water than hens fed corn-soybean meal-alfalfa meal (CSA) diets with either .15, .50, or .75%. NaCl. Moisture content of the hens' feces was not affected by mash or pellet processing of the WM diet. Feeding the .75% NaCl-CSA diet, however, significantly increased fecal moisture beyond that observed with the other treatments. Caged layers fed the WM diet voided more feces (2.6 fold) than did caged layers fed the .50% NaCl-CSA diet, suggesting that wet litter problems observed in the floor pens of birds fed WM were the result of a greater fecal volume voided rather than a higher moisture content per unit of feces.

Animal Feed↗

Improved growth in the progeny of hens immunized with jackbean urease.

Three experiments were conducted with Single Comb White Leghorn and broiler breeder hens. Half of the experimental hens were injected with jackbean urease enzyme and the other half served as uninjected or adjuvant-injected controls. Chicks hatched from urease-injected or control hens were placed factorially (2 x 2) on diets with or without antibiotics. Urease injection of hens resulted in significant improvements in percent fertility and hatch compared with values for control hens. Depending on age, both urease injection and antibiotic feeding stimulated chick growth, independently of one another. Additive effects of these treatments resulted in significant improvements in body weight of chicks injected with urease and consuming antibiotics at all time periods compared with body weights of untreated controls.

Animals↗

Suppressed humoral immunity in chicks fed diets deficient in sodium, chloride, or both sodium and chloride.

Four experiments were conducted to determine the effect of Na and Cl on the antibody response to sheep red blood cells (SRBC). In the first two experiments, Na and Cl were supplemented in the diet together as NaCl at levels from 0 to .75%. In two additional experiments, Na and Cl were supplemented independently; levels varied from .04 to .24% total dietary Na and from .07 to .36% total dietary Cl. Results of the first two experiments indicated that dietary Na and Cl levels above that found in a corn-soybean diet improved the antibody response to SRBC. Additional studies showed that the humoral immunity was significantly suppressed when chicks consumed diets with less than .14% Na and .17% Cl. Increasing dietary Cl from .17 to .27% when dietary Na was .04% suppressed the antibody response. Also, increasing dietary Cl from .21 to .36% when dietary Na was .14 or .24% suppressed the antibody response. The immunosuppression of the humoral response of chicks was determined to be not related to the decreased feed intake resulting from inadequate Na and Cl in the diet.

Animals↗