Core curriculum Nephrology

CKD Part 2

Complications

JM Krzesinski

June 15th 2019

Complications of CKD• Mortality

• AKI

• HTA and CV disease

• CKD metabolic bone disease

• Anemia

• Metabolic acidosis

• Hyperkalemia

• Infection, toxicity of renally excreted drugs (A, G, M)

• Late complications: pericarditis, polyneuropathy, encephalopathy, skin and sexual disorders, bleeding, GI troubles, denutrition, water intoxication

Renal Dysfunction and Increased Cardiovascular Risk

Go et al. NEJM 2004;351:1296

among 1,120,295 US Adults

Cardiovascular Outcomes Worsen With CKD Progression: 3-Y Follow-Up by eGFR Levels

CHF = congestive heart failure.Anavekar et al. N Engl J Med. 2004;351:1285-1295.

0

10

20

30

40

50

60

Composite

End Point

Death From

CV Causes

Reinfarction CHF Stroke Resuscitation

Esti

mate

d E

ven

t R

ate

(%

)

75

60-74

45-59

<45P<0.001

eGFR (mL/min/1.73 m2)

© 2005 The Johns Hopkins University School of Medicine.Post MI

Osteitis fibrosa cystica, adynamic bone disease, osteomalacia, mixed uremic osteodystrophy

Bone pain, fractures mostoften at the dialysis stage

CKD-MBD

Relation withmortality,

inflammation, LVH

FGF23, PTH and Phosphate in CKDIsakova T et al., Kidney Int 2011

Hematological Abnormalities

• Anemia– Chronic blood loss, hemolysis, marrow suppression by

uremic factors, and reduced renal production of EPO

– Normocytic, normochromic

• Coagulopathy– Mainly platelet dysfunction – decreased activity of platelet

factor III, abnormal platelet aggregation and adhesiveness and impaired thrombin consumption

– Increased propensity to bleed – post surgical, GI Tract, pericardial sac, intracranial

– Increased thrombotic tendency – nephrotic syndrome

ANEMIA

Bowry S. and Gatti E., Blood Purification, 2011, 32, 210-219.

ANEMIA(normocytic,

normochromic)

J Lopez Gomez et al., Kidney Int, 2002, 61, suppl 80, S39-S43.

Electrolytic abnormalities

• Hyperkalemia

• Metabolic acidosis

Potassium Imbalance

• Causes of high serum Potassium

– Constipation, dietary intake,

– Protein catabolism, hemolysis, hemorrhage, transfusion of stored blood,

– Metabolic acidosis,

– Drugs: ACE inhibitors, ARBs, B blockers, K sparing diuretics and NSAIDs (but also CNI, Heparin)

– Hyporeninemic hypoaldosteronism: Diabetes, sickle cell disease

Acid Base Imbalance

• Damaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins. – NH3 production is limited because of loss of nephron mass– Decreased filtration of titrable acids – sulfates, phosphates– Decreased proximal tubular bicarb reabsorption – Decreased H+ ion secretion

• Arterial pH: 7.33 - 7.37; serum HCO3 rarely below 15 – buffering offered by bone calcium carbonate and phosphate

Denutrition is a strong risk factor for hospitalization and death

Pallor or sallow-appearing

Ecchymoses, excoriation, uremic frost

Urinous breath fetor, hiccups

Uremic ComplicationsUremic frost

Low testosteronelevel

Follow up of the patients

Susceptibility factors

Initiating factors Stimulating factors of progression

Take home messages

Thank you for your attention

Questions?