Internists, Nephrologist (kidney), Pediatric Specialist
18 years of experience

University Area
4015 Lake Otis Pkwy
Suite 101
Anchorage, AK 99508
907-375-5200
Locations and availability (2)

Education ?

Medical School Score
The University of Texas at Houston (1992)
  • Currently 2 of 4 apples

Awards & Distinctions ?

Awards  
Patients' Choice 5th Anniversary Award (2012)
Patients' Choice Award (2008 - 2012)
Compassionate Doctor Recognition (2009 - 2012)
On-Time Doctor Award (2009)
Associations
American Board of Internal Medicine
American Board of Pediatrics

Affiliations ?

Dr. Gitomer is affiliated with 4 hospitals.

Hospital Affilations

Score

Rankings

  • Alaska Regional Hospital
    2801 Debarr Rd, Anchorage, AK 99508
    • Currently 1 of 4 crosses
  • Providence Alaska Medical Center
    PO Box 196604, Anchorage, AK 99519
    • Currently 1 of 4 crosses
  • Kidney & Hypertension Clinic of Alaska
  • Providence Extended Care Center
    4900 Eagle St, Anchorage, AK 99503
  • Publications & Research

    Dr. Gitomer has contributed to 15 publications.
    Title Giant Cell Tubulitis with Tubular Basement Membrane Immune Deposits: a Report of Two Cases After Cardiac Valve Replacement Surgery.
    Date August 2007
    Journal Clinical Journal of the American Society of Nephrology : Cjasn
    Excerpt

    This paper presents two elderly patients who had normal baseline renal function and had stenotic valvular lesions secondary to rheumatic fever and underwent aortic valve replacements with mechanical valves. Both patients developed acute renal failure after cardiac valve replacement procedures. The renal biopsies revealed acute granulomatous tubulointerstitial nephritis. The unique histologic features were tubular basement membrane (TBM) immune complex deposition detected by both immunofluorescence and electron microscopy and prominent multinucleated giant cells surrounding intact TBM. The temporal relationship to the surgical procedure and the subsequent recovery of the patients' renal functions upon therapy suggested that the renal failure may have been due to an allergic drug reaction from the perioperative exposure to unknown agents, such as prophylactic antibiotics and furosemide. The literature on TBM immune complex deposition was reviewed, and the pathophysiologic mechanisms that may account for the similarities between the clinicopathologic features of these two cases were examined. These two cases expand the histopathologic spectrum of previously described cases of putative drug-induced acute tubulointerstitial nephritis.

    Title Gastrointestinal Symptoms of Henoch-schönlein Purpura Treated with Mycophenolate Mofetil.
    Date October 2006
    Journal Journal of Pediatric Gastroenterology and Nutrition
    Title Treatment of Severe Theophylline Toxicity with Hemodialysis in a Preterm Neonate.
    Date March 2002
    Journal Pediatric Nephrology (berlin, Germany)
    Excerpt

    Theophylline, a drug frequently used to treat apnea of prematurity, has a prolonged half-life of 30 h in neonates. Severe overdoses of theophylline have an associated 10% mortality and significant morbidity. We describe a 1,220-g neonate who developed status epilepticus due to a theophylline overdose. Hemodialysis was instituted to increase elimination of theophylline. The patient tolerated the procedure without complication. The half-life of theophylline was 0.7 h during dialysis. No reported therapies used in neonates have achieved this magnitude of clearance. In fact, the clearance of theophylline in this neonate approached that obtained with hemoperfusion, the standard therapy for theophylline overdose in adult patients. This case demonstrates that hemodialysis is a safe and effective means of enhancing theophylline elimination for neonatal theophylline overdose.

    Title Sch-28080 Depletes Intracellular Atp Selectively in Mimcd-3 Cells.
    Date November 2000
    Journal American Journal of Physiology. Cell Physiology
    Excerpt

    Two H(+)-K(+)-ATPase isoforms are present in kidney: the gastric, highly sensitive to Sch-28080, and the colonic, partially sensitive to ouabain. Upregulation of Sch-28080-sensitive H(+)-K(+)-ATPase, or "gastric" H(+)-K(+)-ATPase, has been demonstrated in hypokalemic rat inner medullary collecting duct cells (IMCDs). Nevertheless, only colonic H(+)-K(+)-ATPase mRNA and protein abundance increase in this condition. This study was designed to determine whether Sch-28080 inhibits transporters other than the gastric H(+)-K(+)-ATPase. In the presence of bumetanide, Sch-28080 (200 microM) and ouabain (2 mM) inhibited (86)Rb(+) uptake (>90%). That (86)Rb(+) uptake was almost completely abolished by Sch-28080 indicates an effect of this agent on the Na(+)-K(+)-ATPase. ATPase assays in membranes, or lysed cells, demonstrated sensitivity to ouabain but not Sch-28080. Thus the inhibitory effect of Sch-28080 was dependent on cell integrity. (86)Rb(+)-uptake studies without bumetanide demonstrated that ouabain inhibited activity by only 50%. Addition of Sch-28080 (200 microM) blocked all residual activity. Intracellular ATP declined after Sch-28080 (200 microM) but recovered after removal of this agent. In conclusion, high concentrations of Sch-28080 inhibit K(+)-ATPase activity in mouse IMCD-3 (mIMCD-3) cells as a result of ATP depletion.

    Title Unexpected Severe Hypocalcemia During Continuous Venovenous Hemodialysis with Regional Citrate Anticoagulation.
    Date April 1999
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Excerpt

    Citrate is known to induce acute hypocalcemia in patients undergoing liver transplantation during the anhepatic phase. We describe the case of a 71-year-old woman with fulminant hepatic failure secondary to hepatitis A, who was started on continuous venovenous hemodialysis (CVVHD) for acute renal failure. Because anticoagulation with heparin was untenable, regional anticoagulation was accomplished by trisodium citrate (46.7%) infusion. Unfortunately, severe hypocalcemia developed when citrate accumulated because of impaired hepatic metabolism. Because of chelation by citrate, the ionized calcium concentration declined to values as low as 2.72 mg/dL (normal, 4.5 to 5.6 mg/dL), whereas the total calcium concentration remained in the normal range. With an unusually high calcium chloride infusion rate via a central line (up to 140 mL/h of 10 mEq/dL CaCl2) and additional boli of CaCl2 (for a total of 190 mEq), the ionized calcium concentration could be maintained at target levels. Nevertheless, the ionized calcium concentration was maintained in the normal range, and the total calcium concentration increased to a value as high as 15 mg/dL. Thus, the total to ionized calcium ratio was 3.5:1. After 24 hours of treatment, trisodium citrate infusion was gradually reduced from 15 mL/h to 7 mL/h, and the calcium chloride infusion was decreased to 50 mL/h. Nevertheless, persistence of the elevated total to ionized calcium ratio (3:1) indicated citrate accumulation likely secondary to decreased hepatic metabolism. Using this approach, the patient was successfully maintained on CVVHD with regional citrate anticoagulation for a total of 11 days without any additional complications. We conclude that CVVHD with regional citrate anticoagulation can be used in patients with acute hepatic failure if increased CaCl2 requirements are anticipated and if citrate is infused at a lower rate compatible with decreased citrate metabolism. Citrate accumulation should be suspected in patients with an elevated total to ionized Ca++ ratio during CVVHD with citrate anticoagulation.

    Title Continuing Medical Education Exercise, April 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, February 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, May 2000.
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, June 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, July 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, August 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, September 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, October 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, November 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    Title Continuing Medical Education Exercise, December 2000
    Date
    Journal American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation

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