Core curriculum Nephrology CKD Part 2 C omplications JM Krzesinski June 15th 2019
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?