Epidemiology
- xxx
Etiology
- xxxx
- xxx
- Toxin
- Cadmium (see Cadmium, [[Cadmium]]), [[Cadmium]])
- Other
- xxx
Physiology
Potential Mechanisms Contributing to Development of Pulmonary Hypertension in ESRD
- 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
Diagnosis
- xxx
Clinical Manifestations
Pulmonary Manifestations
- Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]]): reported in 40% of ESRD patients on chronic HD
Hematologic Manifestations
- Anemia (see Anemia, [[Anemia]])
Neurologic Manifestations
- Posterior Reversible Encephalopathy Syndrome (PRES) (see Posterior Reversible Encephalopathy Syndrome, [[Posterior Reversible Encephalopathy Syndrome]])
Renal Manifestations
Metabolic Acidosis
- 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
Mildly Elevated Osmolal Gap (see Serum Osmolality, [[Serum Osmolality]])
- 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)
Other Manifestations
- Uremic Symptoms
- xxx
Treatment
- xxx
References
- 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