Patients with end stage renal disease (ESRD) on hemodialysis encounter a number of metabolic challenges, including difficulty with glycemic control [1]. Non-diabetic patients with renal failure are prone to hypoglycemia [2,3], and at times, the etiology is difficult to determine. The differential diagnosis of hypoglycemia in the non-diabetic, non-critically ill patient with ESRD is broad including the following: exogenous sulfonylurea or insulin administration, adrenal insufficiency, non-islet cell tumors (tumor production of incompletely processed Insulin like Growth Factor IGF-1 or IGF-2), endogenous hyperinsulinism (beta cell tumors, insulinoma, functional beta cell disorder (nesidioblastosis)), insulin auto-immune hypoglycemia, critical illness, and malnourishment [1]. Additionally, because the kidney is vital for gluconeogenesis and glucose regulation, patients with chronic kidney disease often have compounding problems with glucose homeostasis and hypoglycemia [3,4].

Patients at either extreme of glycemic control are often admitted to ICUs, where tight glycemic control is pursued. In the surgical ICU, strict glycemic control has been shown to improve morbidity and mortality [5]. However, intensive insulin therapy also carries the increased risk of hypoglycemia. In some patients, specifically those in medical intensive care units, this can be associated with worse outcomes [6,7]. Therefore, the reliability of glucose measurements in these clinical scenarios is essential in obtaining glycemic control while minimizing the risk of hypoglycemia.

Point-of-care (POC) glucose testing is commonly used both in outpatient and inpatient settings [8]. Numerous studies have investigated the reliability of POC glucose testing in critically ill patients. While the results in the normal hospital range show accuracy and reliability between POC testing and central laboratory testing, the results are less favorable in critical care settings and at extremes of glycemic control [9].

Overall, the complex clinical presentation, broad differential, and questionable reliability of glucose testing in critical care settings can make the care of a patient with ESRD on hemodialysis challenging.

In this case report, we describe a non-diabetic patient with ESRD on hemodialysis, without a history of glycemic control problems, who developed apparent persistent hypoglycemia as assessed by capillary glucose measurement. Eventually, the apparent hypoglycemia was attributed to discrepant POC and central glucose levels. We use this case as a reminder of the patient safety issues that can arise from the limitations of POC capillary glucose testing, especially in patients with ESRD and/or critical illness.

Our patient is a 75-year-old female with a history of end stage renal disease (ESRD) on hemodialysis (HD), hypertension (HTN), severe aortic stenosis, pulmonary HTN, hypothyroidism, anemia, sacral decubitus ulcers, morbid obesity. She had a rapid decline in health over the preceding six months, including dementia, episodes of sepsis, debilitating arthritis, and gallbladder surgery complicated by kidney failure for which she had become hemodialysis-dependent. On this occasion, she was admitted to the Medical ICU for apparent refractory hypoglycemia observed at a local nursing home. There, her reported blood sugar levels were 20 mg/dl - 40 mg/dl. Per family reports, she did not have a history of diabetes, but had experienced a similar episode of apparent hypoglycemia one month earlier, requiring hospital admission. No further details were available. The nursing home reported symptoms of increased fatigue and questionable mental status changes. However, in the emergency room (ER), she was unable to communicate with staff and was oriented to person only, making determination of changes from baseline difficult. As a result, laboratory testing was heavily relied upon for diagnoses and treatment.

Prior to arrival, she had received intravenous (IV) fluids containing dextrose 5% and 10%. In the ER, initial fingerstick glucose revealed blood sugar of 127 mg/dl, but subsequent sugars were repeatedly <10 mg/dl on fingerstick and as a result, intramuscular glucagon was given. The timing of her last meal was not known. She was eventually started on a glucose drip and admitted to the ICU.

Initial endocrine workup showed low-normal random cortisol, with a normal cosyntropin stimulation test, and a mildly elevated thyroid stimulating hormone, making the diagnosis of panhypopituitarism unlikely. A growth hormone level was not checked. Sulfonylurea and repaglinide levels were negative, ruling out exogenous sulfonylurea or repaglinde administration. IGF-2 level was also normal. Computed Tomography of the pancreas was negative for pancreatic tumor and an octreotide scan was unrevealing for neuroendocrine tumors.

In the midst of the hypoglycemia workup, a discrepancy between glucose values from fingerstick-testing and central venous samples taken from her peripherally inserted central venous catheter (PICC) showed no evidence of significant hypoglycemia. Once this discrepancy was discovered, POC readings were taken only from PICC blood and were more closely concordant with serum glucose levels as measured on the basic metabolic panel.

Her later hospital course was complicated by septic shock from Proteus mirabilis bacteremia. After resolution of this episode, she re-developed a gram-negative rod bacteremia. She was eventually discharged without glycemic problems, but on antibiotics.

Figure 1 above shows the initial discrepancy between capillary glucose and serum glucose measurements in our patient. This discrepancy became less pronounced after approximately Day 8 when most POC glucose values were obtained from central blood.