According to the KDIGO recommendations published in 2012, the absolute indications for initiation of dialysis therapy in patients with end-stage renal failure (ESRD) include at least one of such emerging symptoms as: serositis, electrolyte or acid-base imbalance, uncontrolled volume status or hypertension, pruritus, progressive cachexia refractory to dietary intervention or cognitive impairment (1). These symptoms usually occur when eGFR reaches values between 6 and 10 ml/min/1.73 m². In the clinical practice, the methods most frequently used for eGFR calculation are those based on creatinine serum concentration (Scr) (2). Although CKD-EPI formula is the preferred method for eGFR calculation, MDRD equation is used in the majority of laboratories (3). However, the differences between the results obtained with MDRD and CKD-EPI equations in patients with ESRD are minute.

The credibility of GFR estimation with the MDRD formula is limited. The bias may result from patient’s race or ethnic origin different from the population for which the equation was prepared for. Moreover, the serum creatinine level may be inadequate due to extremely low or high muscle mass, growth, high-protein diet, administration of creatinine preparations, or muscle atrophy (4-6).

These factors may significantly influence the efficacy of dialysis sessions, especially in the view of chronic dialysis therapy, and may result in inadequate prescription of the dialysis dose (7, 8).

This paper presents five of seven cases of patients with indications for chronic dialysis therapy despite low concentrations of markers of kidney failure.

Low serum creatinine concentrations in a patient with low muscle mass – a 96 year old woman with the right kidney cirrhosis and chronic kidney disease probably due to the atherosclerotic vascular nephropathy. Patient’s comorbidities included: arterial hypertension, chronic coronary heart disease with a history of two acute coronary syndromes in 2007 – one of which was an NSTEMI treated with percutaneous coronary intervention with stent placement; tachycardia-bradycardia syndrome with paroxysmal atrial fibrillation and heart failure in the third stage according to the NYHA classification. The patient had been observed in the Nephrology Outpatient Clinic until March 2009 (the creatinine, urea and bicarbonate serum concentrations were 4.1 mg/dl, 95 mg/dl, and 19.8 mmol/l, respectively). As the parameters were stable the patient was diagnosed with CKD stage 5 and was referred for creation of an arteriovenous fistula. The haemodialysis therapy was introduced in June 2009 due to progression of kidney failure and worsening general condition of the patient (creatinine serum concentration 3.98 mg/dl, urea serum concentration 213 mg/dl, bicarbonate serum concentration 14.6 mmol/l). The patient was treated with intermittent dialysis sessions in a schedule 3 times a week for four hours. The dialysis dose measured with Kt/V for urea was 1.28 (table 1, mean value for 6 months of dialysis therapy). The haemodialysis therapy was complicated with an arteriovenous fistula dysfunction in 2012. The fistula was reconstructed several times with the use of PTFE. In April 2013, after another episode of arteriovenous fistula thrombosis and failure in restoring fistula patency, a tunneled, cuffed haemodialysis catheter was implanted into the right jugular vein. Next attempts for the fistula reconstruction were aborted.

During the haemodialysis therapy the patient’s nutritional status maintained stable. With 149 cm height her body mass oscillated around 46 kg – BMI 18.9-22.3. Infrequently, slight oedema of lower legs was observed, while the residual diuresis remained between 1000 and 1500 ml per day on a daily dose of 5 mg of torasemide. The patient used to gain 0-3% of body mass between the dialysis sessions. During the last six months of 2015 the patient’s creatinine serum concentrations fluctuated between 2.23 and 2.75 mg/dl (eGFR 14.01-20.4 ml/min/1.73 m²), urea serum concentration was from 62 mg/dl to 121.9 mg/dl, phosphate serum concentration was between 1.38 and 1.67 mmol/l. Albumin serum concentration maintained in normal ranges – between 3.7 and 4.06 g/dl. nPCR remained on low levels – 0.49-0.8 g/kg/day. Laboratory markers of acid- base imbalance with metabolic acidosis persisted despite dialysis therapy: pH 7.23-7.39, bicarbonate concentration 18.6-27.6 mmol/l.

In September 2015 a significant increase in biochemical parameters was observed after 5 days of dialysis discontinuation (patient’s creatinine serum concentration 3.78 mg/dl, eGFR 11 ml/min/1.73 m², urea serum concentration 135 mg/dl).

In this patient raising the dialysis dose despite low serum creatinine and urea concentrations led to an increase in BMI and albumin concentration, although nPCR levels were low. This proves that the haemodialysis therapy improved protein utilization possibly due to the decreased catabolism secondary to uremic inflammatory reaction.

Low creatinine serum concentrations in a patient with clinical symptoms of cachexia – a 72-year old patient with long-term type 2 diabetes and general arteriosclerotic vascular disease with chronic multivessel coronary artery disease. The patient was admitted to the Cardiology Department in the Priest J. Popiełuszko Bielański Hospital in Warsaw in October 2013 due to exacerbation of a chronic heart failure (NYHA III/IV, EF 25%) in the course of pneumonia. The patient had a history of a myocardial infarction with a consecutive coronary artery bypass graft in 2011 and an external iliac artery angioplasty with stent placement in 2008. During the hospitalization the patient was diagnosed with an advanced renal disease – serum creatinine, urea and albumin concentrations were 3.4 mg/dl, 105 mg/dl and 3.0 g/dl, respectively. Prior to the hospitalization the patient had never been referred to the nephrologist. The attempts of conservative treatment were ineffective, thus, the decision of initiation of the haemodialysis therapy was made. A non-tunneled haemodialysis catheter implanted through the right jugular vein was the patient’s primary vascular access. During the hospitalization the patient’s volume status had improved, however, biochemical renal parameters maintained elevated. The patient was referred for chronic dialysis therapy. A tunneled, cuffed haemodialysis catheter was implanted in December 2013. In February 2014 the patient’s combined urea and creatinine clearance was evaluated after four days of discontinuation of haemodialysis therapy. As the result was 10 ml/min, and the nPCR was 0.79 g/kg/day, with HCO3 18.6 mmol/l we decided to continue the dialysis therapy. In March 2014 an arteriovenous fistula was created on the left forearm. In May 2015 due to the fistula dysfunction another arteriovenous fistula was formed on the left arm.