Chronic Kidney Disease (CKD)

Epidemiology

Pulmonary vasoconstriction (due to hormonal or metabolic derangements), increased CO (due to AV fistula and anemia), diastolic and systolic CHF (increased frequency in CKD patients), and fluid overload

Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]]): reported in 40% of ESRD patients on chronic HD

Posterior Reversible Encephalopathy Syndrome (PRES) (see Posterior Reversible Encephalopathy Syndrome, [[Posterior Reversible Encephalopathy Syndrome]])

Physiology
- Early Chronic Kidney Disease: greater dysfunction in acid excretion than acid anion excretion -> typically have non-anion gap metabolic acidosis (NAGMA) (see Non-Anion Gap Metabolic Acidosis, [[Non-Anion Gap Metabolic Acidosis]]) or anion gap metabolic acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]]) with delta anion gap/delta bicarbonate ratio <1
- Later Chronic Kidney Disease: typically have anion gap metabolic acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]]) with delta anion gap/delta bicarbonate ratio >1

Epidemiology: occurs in CKD with GFR <10 mL/min, without regular hemodialysis
Physiology: due to presence of osmotically-active solute(s)
- Urea
- Unidentified Small Solutes: these are generally cleared with hemodialysis (and are not present in AKI)
Diagnosis: typically results in small osmolal gap (<15-20 mOsm/L)

Yigla M, Nakhoul F, Sabag A, et al. Pulmonary hypertension in patients with end-stage renal disease. Chest 2003;123:1577-82
Nakhoul F, Yigla M, Gilman R, Reisner SA, Abassi Z. The pathogenesis of pulmonary hypertension in haemodialysis patients via arterio-venous access. Nephrol Dial Transplant 2005;20:1686-92