Skip to main content
   COVID-19 Announcement

Hyperbaric Oxygen Therapy Treatment for End Stage Renal Disease

Diabetes kidney disease (DKD) is a leading cause for end stage renal disease in the western world today. If you have found your way to this website, you have done your homework and an extensive amount of reading, I will not bore you by presenting you again with disease processes and the havoc and devastation it causes. As of the date of this writing, there is no treatment that can reverse renal damage.

Hyperbaric oxygen therapy (HBOT) is a process of breathing an increased concentration of oxygen under pressure. The normal atmosphere contains 21 % oxygen, HBOT is a therapy in which the patient breaths concentrations of oxygen up to 99% while in a pressurized vessel, pressurized at a pressure greater than 1ATA or the atmospheric pressure at sea level. Hyperbaric oxygen therapy is generally a safe procedure. Complications are rare. But this treatment does carry some risk. Middle ear injuries can occur. Previous lung injuries and collapse must be ruled out. Hypertension is a contra-indication.

The first thing that occurs is the patients red blood cells become saturated with oxygen. Then plasma, which is the liquid part of the blood then becomes saturated. This enables oxygen to diffuse into tissues compromised by acute inflammation and microvascular disease and dysfunction. These effects have been noted in studies of traumatic brain injuries, wound healing, carbon monoxide poisoning, gangrene infections and oxygen starved tissues (hypoxia) such as diabetic kidneys. In general, some effects of HBOT are seen immediately after treatment, others take numerous treatments.

HBOT enables oxygen to diffuse into tissues compromised by acute inflammation and microvascular disease and dysfunction. This leads to the activation of fibroblasts and mobilization of macrophages and bone marrow–derived vascular endothelial cells. These cellular responses further stimulated neoangiogenesis and vasculogenesis within tissues. These complex cellular and tissue responses are known to support tissue repair and wound healing within chronic ulcerations due to diabetes and radiation tissue injury (Al-Waili and Butler 2006).

Hypoxia is one of the major key dilemmas in the diabetic kidney. Current treatment of diabetic kidney disease relies on nutritional management and drug therapies to achieve metabolic control. To date there have been numerous studies utilizing HBOT in the treatment of DKD or end stage renal failure. The preliminary data supports the concept that HBOT can reduce biomarkers of renal injury, oxidant stress, and mitochondrial dysfunction in patients receiving HBOT while treating diabetic foot wounds. Further studies are needed to confirm these initial findings and correlate them with simultaneous measures of renal function. (Harrison and Giardina 2018). Chronic kidney disease (CKD) is defined as the gradual decline in kidney function (glomerular filtration rate—GFR) over time, affecting nearly 13% of adults (Darshi et al. 2016; Gallagher and Suckling 2016). A pathologic hallmark of DKD is the presence of increased loss of proteins, especially albumin through the renal filtration membrane (glomerulus). The glomerulus is made up of microvasculature and when damaged by years of hyperglycemia, it begins to leak albumin into the urine, a condition known as albuminuria.

Inflammatory hypoxia is recognized as a common barrier to reparative responses in many chronically diseased tissues, from autoimmune inflammatory conditions to chronic wounds and many solid tumors (Eltzschig and Carmeliet 2011; Colgan et al. 2013; Perdrizet 2017). HBOT activates anti-inflammatory mechanisms by suppressing NF-kB expression and reducing levels of TNF and IL-1B. After exposure to HBOT, pro-inflammatory stimulus-induced cytokine production is transiently repressed, whereas cytokine release by unstimulated and lipopolysaccharide challenged macrophages is increased. IFNγ, an anti-angiogenic cytokine, is markedly decreased following HBOT. TNF levels are similarly decreased after HBOT treatment, which helps in the repair following ischemia-reperfusion injury (injury resulting from the return of blood flow to an area that previously lacked blood flow and oxygen). HBOT also works to reduce prostaglandin production, which normally induce inflammation pain, swelling, and increased sensitivity to pain. The inhibition of this PG pathway is therefore hypothesized to play a role in HBOT’s anti-inflammatory effect and ability to reduce pathologic tissue edema (Rachmilewitz et al. 1998).

HBOT also stimulates the production of new blood vessels and their supporting collagenous matrix, by stimulating angiogenesis in response to hyperoxia (Sheikh et al. 2000). HBOT increases localized angiogenic stimuli to mobilize, recruit, and differentiate bone marrow–derived circulating stem and endothelial cells, which promote tissue neoangiogenesis and vasculogenesis.

Conclusion

The effects of HBOT on the kidneys have been noted while treating diabetic foot wounds and has been noted as a side benefit of the treatment. The compromised peripheral tissues can effective be treated and HBOT may eliminate the need for amputation of compromised tissue.

Medicare does not cover the cost of care for a diabetic with peripheral ischemia of the tissues unless the wounds are acute. Medicare will not cover the treatment of HBOT for end stage renal failure. It is imperative that the correct diagnosis by the treating physicians be submitted in order to obtain re-imbursement for insurance carriers. The use of HBOT for the treatment of DKD or end stage renal failure is considered to be experimental. However, the use of HBOT may simply afford the diabetic patient an increase in the quality of life.

Dr. Skaggs is available for consultation by appointment.

Harrison LE , Giardina C, Might hyperbaric oxygen therapy (HBOT) reduce renal injury in diabetic people with diabetes mellitus? From preclinical models to human metabolomics. 2018 J Cell Stress Chaperones 23;6 : 1143-1152. doi: 10.1007/s12192-018-0944-8

Al-Waili NS, Butler GJ. Effects of hyperbaric oxygen on inflammatory response to wound and trauma: possible mechanism of action. Sci World J. 2006;6:425–441. doi: 10.1100/tsw.2006.78.

Al-Waili NS, Butler GJ. Effects of hyperbaric oxygen on inflammatory response to wound and trauma: possible mechanism of action. Sci World J. 2006;6:425–441. doi: 10.1100/tsw.2006.78.

Colgan SP, Curtis VF, Campbell EL. The inflammatory tissue microenvironment in IBD. Inflamm Bowel Dis. 2013;19:2238–2244. doi: 10.1097/MIB.0b013e31828dcaaf. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

Perdrizet G. A. Advances in Experimental Medicine and Biology. Cham: Springer International Publishing; 2017. Chronic Diseases as Barriers to Oxygen Delivery: A Unifying Hypothesis of Tissue Reoxygenation Therapy; pp. 15–20. [PubMed] [Google Scholar]

Perdrizet G. A. Advances in Experimental Medicine and Biology. Cham: Springer International Publishing; 2017. Chronic Diseases as Barriers to Oxygen Delivery: A Unifying Hypothesis of Tissue Reoxygenation Therapy; pp. 15–20. [PubMed] [Google Scholar]

Sheikh a Y, Gibson JJ, Rollins MD, et al. Effect of hyperoxia on vascular endothelial growth factor levels in a wound model. Arch Surg. 2000;135:1293–1297. doi: 10.1001/archsurg.135.11.1293. [PubMed] [CrossRef] [Google Scholar]

Darshi M, Van Espen B, Sharma K. Metabolomics in diabetic kidney disease: unraveling the biochemistry of a silent killer. Am J Nephrol. 2016;44:92–103. doi: 10.1159/000447954. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

Gallagher H, Suckling RJ. Diabetic nephropathy: where are we on the journey from pathophysiology to treatment? Diabetes Obes Metab. 2016;18:641–647. doi: 10.1111/dom.12630. [PubMed] [CrossRef] [Google Scholar]