clinical management of anaemia in a patient with chronic kidney disease not- on-dialysis jolanta...

Clinical management of anaemia in a patient with chronic kidney disease not-on-dialysis

Jolanta Malyszko, MD

Department of Nephrology and Transplantology

Medical University of Bialystok, Poland

© Springer Healthcare, a part of Springer Science+Business Media; 2010.

http://www.springerhealthcare.com/

http://www.springer.com/?SGWID=0-102-0-0-0

Objectives

● Focus on anaemia in CKD and DM, including prevalence and outcome

● Case report: Diagnosis of anaemia● Treatment: Iron supplementation and ESA therapy● Hb variability: Practical considerations● Safety issues with ESA therapy

CKD: chronic kidney disease; DM: diabetes mellitus; Hb: haemoglobin; ESA: erythropoiesis-stimulating agent


CKD anaemia: A common complication

● Anaemia associated with CKD is a major complication even in early stages

● Hb decreases progressively with the degree of renal impairment1

● CKD anaemia occurs earlier in patients with type 2 diabetes2

1. Jungers. Nephrol Dial Transplant 2002; 17:1621-27, 2. Joss, et al. QJM 2007;100:641-47

CKD: chronic kidney disease; Hb: haemoglobin


Multiple choice question 1

Which of the following statements are true?

1.Anaemia associated with CKD is a major complication even in its early stages.

2.Haemoglobin remains stable despite the degree of renal impairment.

3.Among patients with diabetes, CKD anaemia occurs earlier than among non-diabetics.

A: 1

B: 1 & 3

C: All of the above

D: None of the above

© Springer Healthcare, a part of Springer Science+Business Media; 2010.CKD: chronic kidney disease

CKD anaemia with diabetes

<3030-6060-90>90

0

60

45

15

Stage 2

Stage 3Stage 4+

Stage 130

eGFR (mL/min/1.73m2)

Prev

alen

ce a

naem

ia (%

)

microalbuminuria

macroalbuminuria

normoalbuminuria

Adapted from Thomas, et al. Nephrol Dial Transplant 2004; 19:1792-97

Correlates with eGFR

eGFR: estimated glomerular filteration rate


Case report

• Caucasian female born in 1956, high-school teacher• Type 2 DM diagnosed at 33 years of age, treated with

metformin (850 mg tid) and glimepiryde (3 mg qd)• Surgery for ovarian abscess at 44 years of age• Problems with blood pressure control at 45 years of age• Under diabetologist care

DM: diabetes mellitus; tid: 3 times a day; qd: once a day


Nephrology findings

• 1st nephrology consultation at 50 years of age (Oct 2006) owing to poor blood pressure control

• Creatinine: 1.07 mg/dL; Hb: 12.6 g/dL, Hct: 38%; total cholesterol: 233 mg/dL

• Other medications: Indapamide SR; simvastatin 20 mg bedtime; quinalapril 5 mg

• ABPM: Mean SBP 162 mgHg; mean DBP 91 mmHg; non dipper

• Urinary protein excretion: 3.4 g/d

ABPM: ambulatory blood-pressure monitoring; SBP: systolic blood pressure; DBP: diastolic blood pressure


Additional findings and recommendations

• Leg oedema• Urinary glucose: 0.26g/L• Potassium: 5.46 mmol/L; sodium: 141 mmol/L• TSH: 1.449 mIU/L• Quinapril: ↑10 mg qd• Add telmisartan: 80 mg qd • Furosemide: 40 mg qd • Refused insulin therapy

TSH: thyroid-stimulating hormone; qd: once a day


1st nephrology hospitalisation

• 51 years of age (Dec 2007), owing to nephrotic syndrome, UAE- 8 g/d; albumin: 2.6 g/dL; protein: 5.5 g/dL

• Fasting glucose: 255 mg/dL; 2h post-meal: 280 mg/dL; urinary glucose: 250-1454 mg/dL; creatinine: 1.26 mg/dL; eGFR (MDRD): 48 mL/min

• Hb: 10.5 g/dL; Hct: 30.7%; MCV: 84.8 fl• CRP: 1.3 mg/L• Chol: 200 mg/dL; TG: 177 mg/dL• Simple diabetic retinopathy• Antihypertensives continued, insulin therapy refused• Oral iron started

UAE: urinary albumin excretion; eGFR: estimated glomerular filtration rate; MDRD: modification of diet in renal disease; Hb: haemoglobin; MCV: mean corpuscle volume; CRP: c-reactive protein; TG: triglyceride


Outpatient unit

● March 2008: Hb 10.8 g/dL; oral iron ● June 2008: Iron: 56 μg/mL; TIBC: 263 μg/mL; TSAT: 21%;

Ferritin: 241.41 ng/mL; Hb: 9.0 g/dL; Hct: 26.4%; plt: 464 x 103/mL; WBC: 11.26x106/mL; CRP: 0.2 mg/L; creatinine: 1.88 mg/dL; eGFR: 34 mL/min

Darbepoetin (20 μg) Q2W then 40 μg QM Hb rose to 9.8 g/dL then 10.5 g/dL after 4 months

Hb: haemoglobin; TIBC: total iron binding capacity; TSAT: transferrin saturation; Hct: haematocrit; eGFR: estimated glomerular filteration rate; Q2W: once every 2 weeks; QM: once a month; CRP: C-reactive protein; WBC: white blood cells; Hct: haematocrit


2nd nephrology hospitalisation

● Dec 2008: fall in Hb despite ESA therapy● Hb: 8.5 g/dL; Hct: 25.6 %● Ferritin: 104 ng/mL; TSAT: 21%; CRP: 2.2 mg/L;

creatinine: 1.96-3.28 mg/L; eGFR (MDRD): 16-28 mL/min; urinalysis protein: 100 mg/dL; glucose: 363 mg/dL; albumin: 3.4 g/dL; tprotein: 6.7 g/dL

● IV iron and ESA continued

ESA: erythropoiesis-stimulating agent, eGFR: estimated glomerular filteration rate, MDRD: modification of diet in renal disease; tprotein: total protein; CRP: C-reactive protein; Hct: haematocrit; Hb: haemoglobin; TSAT: transferrin saturation


3rd nephrology hospitalisation

• Feb 2009: Hb 10.2 g/dL; April Hb: 11.5 g/dL; darbepoetin alfa: 40 μg/month

• May 2009: 3rd nephrology hospitalisation• Hb: 9.2 g/dL; CRP: 0.4 mg/dL; Fe: 35 μg/dL; TSAT: 14%;

ferritin: 131 ng/mL; CEA: 2.5 ng/mL (N: 0-3 ng/mL); Ca-125: 237 mIU/mL; (N: 0-35 mIU/mL), tprotein: 7.1 g/dL; creatinine: 4.21 mg/dL

• Insulin therapy introduced• Ascites, ovarian tumour: surgery • Ovariectomy and hysterectomy: ovarian cystadenoma

Hb: haemoglobin, CRP: C-reactive protein, Fe: iron, TSAT: transferrin saturation, CEA: carcinoembryonic antigen, Ca: calcium


Post-surgical course

• IV iron supplementation• Creatinine: 2.1-2.92 mg/dL; eGFR: 18-26 mL/min• Hb: 9.8 g/dL; after 1 g of IV iron ESA reintroduced in

June 2009 • Creatinine stable 2.56-2.80 mg/dL• Hb rose to 11.5 /dL (August 2009), then 12.2 g/dL;

darbepoietin alfa dose 20 μg/month, then Hb 11.7 g/dL (Oct 2009), continue ESA 20 μg/month

• Hb stable: 11.9-11.8 g/dL

Hb: haemoglobin; ESA: erythropoiesis-stimulating agent; eGFR: estimated glomerular filteration rate


Multiple choice question 2

The patient’s haemoglobin has reached 13.2 g/dL; she asks her physician whether her ESA therapy should be continued. Your possible answer is:

A: As her quality of life has improved, I would continue ESA therapy

B: I would lower the dose of ESA by 25%

C: I would discontinue ESA therapy

D: None of the above


Safety considerations

● Cystadenoma: Continue with ESA? – IV iron without an ESA results in a fall in Hb

● Continue with careful gynaecological monitoring

ESA: erythropoiesis-stimulating agent


Conclusions

● ESA therapy is effective in the clinical management of CKD

● Darbepoetin alfa administered monthly was effective and Hb levels were stable

● In patients with a history of malignancy, periodic monitoring is warranted

ESA: erythropoiesis-stimulating agent; CKD: chronic kidney disease; Hb: haemoglobin


clinical management of anaemia in a patient with chronic kidney disease not- on-dialysis jolanta...

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