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Increased Hematocrit During Sodium-Glucose Cotransporter 2 Inhibitor Therapy
Indicates Recovery of Tubulointerstitial Function in Diabetic Kidneys
#MMPMID27829948
Sano M
; Takei M
; Shiraishi Y
; Suzuki Y
J Clin Med Res
2016[Dec]; 8
(12
): 844-847
PMID27829948
show ga
Sodium-glucose cotransporter 2 (SGLT2) inhibitors have been attracting attention
for cardiovascular as well as antidiabetic effects since the results of the
Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus
Patients (EMPA-REG OUTCOME Trial) were reported. The hematocrit increases during
treatment with SGLT2 inhibitors, which have a diuretic effect but do not cause
sufficient hemoconcentration to increase the risk of cerebral infarction.
Elevation of the hematocrit during SGLT2 inhibitor therapy is presumed to involve
enhancement of erythropoiesis in addition to hemoconcentration. In patients with
diabetes, the erythropoietin level increases after initiation of treatment with
the SGLT2 inhibitor dapagliflozin and reaches a plateau in 2 - 4 weeks. The
reticulocyte count increases simultaneously, followed by elevation of hemoglobin
and hematocrit. In patients with diabetes, the proximal tubules are overtaxed by
excessive glucose reabsorption and the increased oxygen requirement causes
tubulointerstitial hypoxia. Consequently, erythropoietin production is impaired
because "neural crest-derived" fibroblasts surrounding the damaged renal tubules
undergo transformation into dysfunctional fibroblasts. SGLT2 inhibitors reduce
the workload of the proximal tubules and improve tubulointerstitial hypoxia,
allowing fibroblasts to resume normal erythropoietin production. These drugs
represent a new class of diuretics that have a renoprotective effect by improving
tubulointerstitial hypoxia, which is the final common pathway to end-stage renal
disease. In patients with diabetes, elevation of hematocrit may be a surrogate
marker for recovery from reversible tubulointerstitial injury.
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