Clinical Year in Review: Nephrologie
Dr. B. Vogt, Néphrologie/Hypertension, CHUV-UniL, Lausanne
1. Renal anemia :
All patients with chronic anaemia associated with chronic kidney disease (CKD)
should be investigated for possible treatment, irrespective of the stage of kidney
disease and requirement for renal replacement therapy.
Patients with CKD and haemoglobin (Hb) concentration:
< 11.5 g/dl in adult female patients
< 13.5 g/dl in adult male patients
< 12.0 g/dl in adult male patients aged >70 years.
Assessment of anaemia:
Hb, Hct
absolute reticulocyte count
ferritin concentration
And one of the following parameters:
transferrin saturation (TSAT)
percentage of hypochromic red blood cells (HRC)
reticulocyte Hb content (CHr)
And to assess inflammation:
CRP (or haptoblogine)
A more extensive work-up of anemia at the beginning of therapy may include:
- assessment of occult gastrointestinal blood loss
- vit. B12 and folate
- iPTH
- differential white blood count and platelets
- protein electrophoresis/immunoblotting
In selected cases further investigations (bone marrow etc.).
No value of plasma erythropoietin levels – do not measure it !
Diagnosis of anaemia due to erythropoietin deficiency:
1. significant impairment of renal function
AND
2. no cause for anaemia other than chronic kidney disease (CKD)
Mortality/morbidity increases with low haemoglobin (below 11 g/dl), and probably
also with high haemoblobin levels, in patients with chronic kidney disease. Reasons not
clear.
Haemoglobin target levels patients with chronic kidney
disease (CKD) :
Hb > 11 g/dl (Hct > 33%)
Hb < 13 g /dl (< 12 g/dl aux USA).
Recommendation: reach this target within 4 months of starting treatment.
Anaemia correction with rHu EPO in HD-CKD patients:
First, assess iron stores and, if necessary, consider iron deficiency correction, usually
with iv iron to be more effective in same time period.
The study “Erythropoietic Response and Outcomes in Kidney Disease
and Type 2 Diabetes” by Pfeffer MA, at al. N Engl J Med. 2009; 361:2019-32, and
Solomon SD, et al. N Engl J Med 2010;363:1146-55, showed that too High haemoglobin
Under correction is associated with increased stroke rate.
2. Iron Therapy
The greatest impact of IV iron is on EPO usage.
Aim of iron supplements:
-Serum ferritin level >200 µ/L in CKD patients not on dialyses
-Serum ferritin level 200–500 µ/L both HD patients and PD patients
AND
-TSAT >20% (unless ferritin >800 µ/L)
OR
-Percentage hypochromic red blood cells (HRC) <6% (unless ferritin >800 µ/L)
In practice, it is likely this will require IV iron.
Different iron preparations:
- Iron sucrose (Venofer®)
- Sodium ferric gluconate (Ferrlecit®)
- High MW dextran (Dexferrum®)
- Low MW dextran (Infed®)
- Ferric carboxymaltose (Ferinject®), for ex.: 100 mg iv
3. Controle of Calcium-Phosphate in Patients with chronic kidney disease
not on dialyses:
1. Dose vitamin D 25-OH and 1,25-OH, calcium, phosphate and iPTH.
2. Substitute vitamin D 25-OH and/or 1,25-OH accordingly, control calcium!
3. If phosphate elevated, start with Ca-based, PO4 binders.
4. Non Ca-based PO4 binders and cinacalcet:
- very interesting substances
- expensive, usually not payed by insurance company
- studies missing in predialyses patients
4. Lipids in chronic kidney disease
History:
4D and AURORA lipid lowering no effect on mortality
in dialyses patients.
SHARP study:
The results of the Study of Heart and Renal Protection:
Results should be published these days.
2/3 of patients (6247) not yet on dialyses at beginning of
the study.
9438 patients, CKD not on dialyses, randomized placebo (4620)
vs ezetimide/simvastatine (4620).
1-year LDL-C reduction of 30 mg/dL with simvastatin 20 mg alone
and of 43 mg/dL with eze/simvastatine 10/20mg
(Am Heart J 2010;0:1-10.e10)
Key outcome: Major atherosclerotic events (coronary death, MI,
non-haemorrhagic stroke, or any revascularization)
At 5-years: 17% risk reduction (35 mg/dl LDL-C reduction)
5. The 10 POINTS of NEPHRON - PROTECTION
1.
Nephropathy: diagnosis and therapy
2.
Controle renal anemia: Hb 11 – 12 (13) g/dl
3.
Controle Ph x Ca, iPTH, consider bicarbonate
4.
Controle blood pressure: < 125/85 mm Hg in proteinuria
5.
Target proteinuria: < 0.3 g/24 h
6.
Controle lipids
7.
Controle HbA1c in diabetes: < 7.5%
8.
Stop smoking
9.
Decrease salt intake
10.
Exercise, weight loss if indicated
6. Idiopathic Membranous Nephropathy (Glomérulonéphrite extramembraneuse)
Principal lesion: podocyte and glomerular basale membrane (GBM)
Mechanisms: Autoimmun - in situ formation of Ag-Ac complexes
Ethiology: Idiopathic or secondary GN. Secondary to: cancer, drugs (NSAID), hepatitis,
etc.
Clinical: Nephrotic syndrome (oedema); Proteinuria > 2.5 – 3.5 g/24h,
hypoalbuminemia ≤ 30 g/l.
a. Treatment NON immunosuppressive:
The 10 points of Nephron Protection: Blood pressure, anemie, Ph and Ca, etc.
b. Treatment immunosuppressive:
- steroïdes at high dose, AND
- cyclophosphamide, or cyclosporine
 important side effects
Consider rituximab (MabThera).