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Biomedical subjects

K A Kirchner

Publications and source records attributed to K A Kirchner.

At least 55 records · Page 3Linked to original sources
PubMed1987

CAPD patients as renal transplant patients.

Most authors state that the continuous ambulatory peritoneal dialysis (CAPD) patient is not at increased risk when transplanted. These patients are always exposed to the risk of peritonitis, which may increase if patients are peritoneally dialyzed while immunosuppressed. The postoperative course of patients transplanted from our CAPD program from 1979 through August 1985 was evaluated. The transplant survival of patients dialyzed by CAPD, home hemodialysis, and at a free-standing dialysis facility were compared. Pretransplant dialysis modality did not influence long-term transplant success. Three of seven patients who required dialysis postoperatively developed peritonitis. The dialysis catheter was removed in two patients and one was treated by lavaging the peritoneal cavity with antibiotics. There was one instance of dialysate leaking through a drain in the transplant bed. This patient was converted to hemodialysis for subsequent dialysis. The dialysis catheters were removed at the time of discharge from hospital. Literature review confirmed this experience. Peritoneal dialysis post-transplant exposes the patient to a 10-33% risk of peritonitis and a 10% risk of a wound complication. Peritoneal dialysis patients are subject to risks unique to peritoneal dialysis. These complications do not translate into excessive morbidity or graft loss.

Adolescent↗
PubMed1987

Lithium as a marker for proximal tubular delivery during low salt intake and diuretic infusion.

Fractional lithium clearance (CLi/CIn), transit time occlusion time (e-TT/OT), and late proximal tubule fluid-to-plasma inulin ratio [1/(TF/P)In] determined by micropuncture were measured in the same kidney during 5-sec-butyl-5-ethyl-2-thiobarbituric acid (Inactin) anesthesia in rats fed either less than 2 mu eq sodium/g diet, rodent chow containing 20 mu eq sodium/g diet, or rodent chow and 0.5% NaCl to drink. Both CLi/CIn vs. e-TT/OT (r = 0.59) or 1(TF/P)In (r = 0.65) were linearly correlated at all sodium intakes. Quantitative estimates of proximal delivery by 1/(TF/P)In and e-TT/OT were similar (P = NS), whereas estimates from CLi/CIn were lower (P less than 0.05 or less) than the direct methods even when corrected for pars recta reabsorption. After acetazolamide or amiloride, but not furosemide, all methods for proximal delivery correlated quantitatively (P = NS) in sodium-restricted rats. Between amiloride and nondiuretic sodium-restricted rats, 1/(TF/P)In was not different. Proximal delivery estimated by CLi/CIn slightly (P = NS) underestimated direct measurements during 2% volume expansion [fractional sodium excretion (FeNa) 0.65 +/- 0.08%]. Thus, in the rat, CLi/CIn is not a quantitative estimate of proximal delivery if FeNa is less than 0.65% due to distal lithium reabsorption. CLi/CIn determined after amiloride may provide a correct estimate of proximal delivery during sodium restriction.

Animals↗
PubMed1987

Indomethacin antagonizes furosemide's intratubular effects during loop segment microperfusion.

To determine if indomethacin antagonizes the effect of intraluminal furosemide, superficial loop segments were microperfused from latest proximal to earliest distal tubules at 20 nl/min with 10(-5) M furosemide in rats treated with indomethacin or vehicle. Base-line loop chloride reabsorption was determined in the presence and absence of indomethacin in a third and fourth group perfused with a similar solution with furosemide omitted. Arterial pressure, whole kidney inulin clearance and urinary chloride excretion were not different among groups. Fractional loop chloride reabsorption was less (P less than .05) in vehicle-treated rats perfused with furosemide than in time control rats perfused without furosemide (30.8 +/- 2.8 vs. 50.3 +/- 2.8%). Fractional chloride reabsorption was greater (P less than .05) in furosemide-perfused loops of indomethacin-treated rats than furosemide-perfused loops of vehicle-treated rats (44.2 +/- 1.9 vs. 30.8 +/- 2.8%). Addition of 10(-4) M prostaglandin E2 to perfusate did not potentiate furosemide's effect in vehicle-treated rats but restored furosemide's potency in indomethacin-treated rats. Thus, indomethacin had no effect on base-line loop chloride uptake but attenuated furosemide's luminal effect. This response could be reversed by luminal prostaglandin E2. This study demonstrates that indomethacin antagonizes furosemide's tubular effects in the absence of furosemide-induced vasodilatation.

Absorption↗
PubMed1986

Prostaglandin E2 but not I2 restores furosemide response in indomethacin-treated rats.

Indomethacin attenuates furosemide's natriuretic response. Although this has been attributed to cyclooxygenase inhibition, attempts to correlate prostaglandin (PG) production with furosemide's natriuresis have led some investigators to conclude that prostaglandins are not involved in this response. This study was designed to evaluate the effects of intraaortic administration of PGE2, PGI2 (100 ng X kg-1 X min-1), or the vasodilators secretin or bradykinin (75 microU X kg-1 X min-1) on the furosemide-indomethacin antagonism. Fractional sodium excretion (FENa) during furosemide administration was 4.59 +/- 0.50% in control rats but 1.84 +/- 0.33% in indomethacin-treated rats (Indo) (P less than 0.001). PGE2 prevented indomethacin from attenuating furosemide's response (FENa, 3.91 +/- 0.25%; P = NS vs. control; P less than 0.01 vs. Indo). PGI2, however, failed to prevent the furosemide-indomethacin antagonism (FeNa, 1.94 +/- 0.59%, P less than 0.001 vs. control; P = NS vs. Indo). Inulin clearance, arterial pressure, filtered sodium load, and renal blood flow were not different between groups. Neither secretin nor bradykinin prevented the indomethacin-furosemide antagonism. This study is consistent with the hypothesis that indomethacin antagonizes furosemide's natriuretic response by prostaglandin synthesis inhibition. Furthermore, PGE2 seems to restore furosemide's response through actions other than a vasodilatory effect.

Animals↗
PubMed1985

Role of prostaglandins in renin suppression during acute potassium loading.

Acute K loading suppresses plasma renin activity (PRA) and may alter prostaglandin biosynthesis. To determine whether the effect of K on PRA was modulated through changes in the prostaglandin system, dietary NaCl-restricted rats were infused with prostaglandin I2. PRA was then determined before and 90 min after a KNO3 infusion. Control rats received only the prostaglandin infusion. PRA increased in rats receiving prostaglandins alone. K loading prevented the increase in PRA. To further exclude prostaglandins in PRA suppression during K loading, the effects of K on PRA were determined during prostaglandin inhibition with meclofenamate or indomethacin. K loading also suppressed PRA during prostaglandin inhibition. In neither study could the changes in PRA be attributed to changes in mean arterial pressure, glomerular filtration rate, plasma volume expansion, or urinary NaCl excretion rate. We conclude that the effects of K on PRA are independent of the prostaglandin system.

Animals↗
PubMed1985

Prostaglandin inhibitors alter loop segment chloride uptake during furosemide diuresis.

Prostaglandin synthesis inhibition antagonizes the chloruretic effect of furosemide. To identify the site of this interaction, cortical micropuncture was performed in furosemide-treated rats during meclofenamate or indomethacin infusion. Control rats received the vehicle for prostaglandin synthesis inhibition. The fractional excretion of chloride decreased from 10.6 +/- 1.0% in control rats to 6.5 +/- 0.93% in indomethacin-treated rats (P less than 0.01) and to 5.7 +/- 0.7% in meclofenamate-treated rats (P less than 0.001). Mean arterial pressure, inulin clearance, renal blood flow, and single nephron glomerular filtration rate were not different among the groups. Chloride delivery out of the late proximal tubule was also not different among the groups. Early distal tubule chloride delivery was greater (P less than 0.001) in control rats than in either prostaglandin-inhibited group. Late distal chloride delivery was also greater in control rats. Calculated loop segment chloride uptake was 9 +/- 2% in furosemide-treated control rats but 18 +/- 2% in both indomethacin- and meclofenamate-treated rats (P less than 0.05). Distal tubule chloride uptake was greater in control than in prostaglandin-inhibited rats. Thus, the attenuated chloruretic response to furosemide observed in indomethacin- or meclofenamate-treated animals may in part result from increased chloride uptake in the loop segment of superficial nephrons.

Animals↗
PubMed1985

Protection from ischemic renal injury by fructose-1,6-diphosphate infusion in the rat.

Fructose-1,6-diphosphate (FDP) improves survival in experimental shock. To determine if FDP would protect against single organ damage, rats pretreated with an intravenous infusion of 5% FDP were subjected to 30 minutes of bilateral renal artery occlusion. Controls received an equal volume of a dextrose and sodium chloride solution. Renal function and histology were examined in all groups 24 hours after the insult. Following ischemia, FDP-treated rats had inulin clearances (FDP 897 +/- 129 vs control 349 +/- 59 microliter/min/100 gm BW; P less than 0.01) and solute excretion rates (FDP 6,386 +/- 1,346 vs control 2,602 +/- 396 mOsm/kg/min/100 gm BW; P less than 0.05) greater than control and not different (P-NS) from sham-operated rats. Renal histology was better preserved in the FDP-pretreated group. Thus, pretreatment with FDP provides histologic and functional protection from an ischemic renal insult.

Animals↗
PubMed1984

Long-term hemodialysis at reduced dialysate flow rates.

20 stable hemodialysis patients were maintained on a dialysate flow rate of 300 ml/min (QD 300) to determine the safety of prolonged reductions in dialysate flow rate. After 24 months, QD 300 compared to QD 500 resulted in no change in weight, blood pressure, BUN, hematocrit, creatinine, bicarbonate, potassium, cholesterol, or calcium. Serum phosphate concentration increased between month 13 and month 17 but then stabilized. No adverse symptoms developed. EEGs and motor nerve conduction studies following 24 months at QD 300 were normal. We conclude that QD 300 does not impair dialysis efficiency for most small molecules and saves $1.38 per patient per dialysis.

Adult↗
PubMed1983

Effect of acute potassium infusion on loop segment chloride reabsorption in the rat.

To assess the effect of acute potassium loading on proximal tubule and loop chloride handling, chloride transport was examined in superficial cortical nephrons in control rats and after infusion with either 0.3 M KNO3 (KVE) or 0.3 M NaNO3 (NaVE) using micropuncture techniques. Infusion with either salt increased plasma volume, single nephron glomerular filtration rate (SNGFR), and delivery of fluid and chloride out of the proximal tubule. Plasma volume, tubule fluid-to-plasma inulin ratio, proximal transepithelial chloride ratio, and absolute and fractional proximal chloride delivery, however, were not different in the NaVE and KVE groups. Early distal tubule fluid flow rate, SNGFR, and fluid reabsorption were greater than control values following either infusion but these were not different between KVE and NaVE. Early distal tubule chloride concentration and transepithelial chloride gradient were greater and fractional chloride reabsorption was less in KVE than in either control or NaVE groups. Calculated fractional loop segment chloride reabsorption was less in KVE animals. These data suggest that potassium loading reduces fractional chloride reabsorption in the loop segment of rat superficial cortical nephrons.

Animals↗
PubMed1983

Chronic granulocytic leukemia after renal transplantation.

Chronic granulocytic leukemia (CGL) developed in a 31-year-old man after he underwent a third renal transplant. The leukemia was initially controlled with azathioprine sodium and prednisone therapy, but eventually it entered blast cell crisis. This was controlled with an adult acute lymphocytic leukemia protocol with an excellent response. Despite discontinuing treatment with azathioprine and with the use of busulfan to control the peripheral WBC count, the patient maintained stable renal function for one year following treatment of the blast cell crisis and subsequently died of sepsis. We suggest that CGL after renal transplantation is similar to that observed in the general population and can be treated with the usual chemotherapeutic agents for the disorder without sacrificing renal function.

Adult↗
PubMed1982

Effects of acute potassium infusions with salts other than chloride on plasma renin activity.

To evaluate the contribution of chloride to the suppression of plasma renin activity (PRA) by KCl, PRA was measured before and after venous infusions of KCl, KHCO3, KNO3, and KC2H3O2 in dietary NaCl-restricted rats. In contrast to controls, PRA decreased (P less than 0.02) after infusion of each potassium salt [KCl from 55.3 +/- 6.4 to 27.0 +/- 6.4 ng.ml-1.h-1 (mean +/- SE); KC2H3O2 from 39.3 +/- 4.0 to 20.6 +/- 4.0; KHCO3 from 64.4 +/- 6.2 to 47.2 +/- 6.2; KNO3 from 40.0 +/- 4.0 to 18.6 +/- 4.0]. Arterial pressure, plasma volume, inulin clearance, serum sodium concentration, and net sodium balance were not different between control and potassium-infused groups. Potassium loading did not increase absolute or fractional sodium excretion. PRA failed to decrease in animals given an equal volume of NaNO3. Furosemide prevented the fall in PRA associated with potassium loading despite replacement of urinary losses. These results suggest that the decrease in PRA observed during potassium loading occurs through the macula densa mechanism but is not dependent on concomitant chloride administration. As furosemide prevents the fall in PRA, macula densa chloride transport may be necessary for potassium to exert this effect.

Animals↗
PubMed1982

Hereditary thrombotic thrombocytopenic purpura: microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency occurring in consecutive generations.

Microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency occurred in a mother an daughter when each was in her third decade. The mother had prominent neurological findings, fever, and expired from renal insufficiency. Her daughter's only major symptom was renal insufficiency. The similarity of the mother's illness to thrombotic thrombocytopenic purpura and of the daughter's to adult hemolytic uremic syndrome suggests that these diseases are variants of a single clinical disorder, while their occurrence in direct descendents strengthens the postulate that in selected instances a genetic predisposition to these disorders may be important.

Adult↗
PubMed1982

Improvement in disequilibrium symptoms during dialysis with low glucose dialyzate.

This study compares the frequency of dialysis disequilibrium symptoms (DDS), in 17 stable non-diabetic chronic hemodialysis patients, during a period using low glucose (200 mg/100 ml) dialyzate to a similar period using a glucose free dialyzate. There was a significant decrease in the total number of symptoms as well as the frequency of headache and post-dialysis fatigue during the low glucose period as compared to the glucose free period. The decrease in nausea or vomiting, and cramps was not significant while frequency of hypotension was unchanged. Evaluation of serum sodium, potassium, BUN, glucose and osmolarity did not reveal significant differences during the two periods. Dialysis with a low glucose bath produces less DDS than glucose free dialyzate.

Blood Urea Nitrogen↗
PubMed1981

Effect of hypochloremia on loop segment chloride and solute reabsorption in the rat during volume expansion.

Hypochloremia has been associated by inference from clearance studies with disturbances in free water reabsorption and renal renin release by a macula densa mechanism. To examine directly these relationships, we studied chloride, fluid, and solute transport in the loop segment (LS) of rat superficial nephrons by micropuncture techniques following acute volume expansion with 0.15 m sodium chloride (CVE) or sodium bicarbonate (BVE). Plasma renin activity was suppressed in group CVE but not in group BVE. Blood pressure, plasma volume expansion, whole kidney GFR, urinary sodium excretion, late proximal and early distal SNGFR, and fluid delivery to the LS were no different between groups CVE and BVE despite different plasma chloride concentrations (102 +/- 5 mEq/liter for CVE vs. 74 +/- 3 for BVE; P less than 0.001). Absolute LS chloride reabsorption was less in BVE than it was in CVE (2030 +/- 120 pEq/min vs. 2454 +/- 136; P less than 0.025). This was associated with significantly lower fractional absolute LS solute reabsorption and higher early distal tubule fluid osmolality. These data demonstrate directly and in vivo that a decrease in chloride reabsorption in the LS of superficial nephrons is associated with impaired solute reabsorption in that segment and a failure to suppress plasma renin activity by sodium loading.

Absorption↗
PubMed1980

Factors influencing chloride reabsorption in the collecting duct segment of the rat.

To study factors influencing Cl reabsorption in the collecting duct segment of the rat, excretion of Cl and of 36Cl injected into late distal tubule segments of superficial nephrons were examined by microinjection and free-flow micropuncture techniques. Selective dietary Cl restriction for 7-10 days decreased urinary 36Cl recovery for microinjection [74 +/- 5% (SE)] compared with normal rats (90 +/- 3%, P < 0.01). Infusion of 0.15 M NaHCO3 (10% body wt) in the Cl-restricted rat led to marked increases in urinary flow rates and sodium excretion but did not increase 36Cl recovery. In these NaHCO3-infused rats, recovery of 36Cl was unaffected by increasing Cl concentration in the injectate from 40 to 140 peq/nl, but increased to levels not different from control (89 +/- 3%) when amphotericin B was included in the injectate. Equivalent infusion of 0.15 M NaCl in the Cl-restricted rats also increased 36Cl recovery to control levels (89 +/- 3%). This response was not altered by administration of DOCA. Absolute chloride delivery to late distal tubule sites was not different in NaCl- and NaHCO3-expanded groups, and (TF/UF)Cl was less in the NaHCO3 group (0.27 +/- 0.03 vs. 0.37 +/- 0.02, P < 0.05); therefore, the chemical gradient for Cl did not favor Cl efflux. There was a significant correlation between urinary recovery of 36Cl and urinary Cl excretion in the NaCl- and NaHCO3-expanded animals. It is suggested that Cl restriction alters, by an as yet unknown mechanism that is independent of changes in Na balance, the intrinsic Cl-absorbing capacity of the collecting duct.

Animals↗