- Acidosis consider HCO3, if hypoCa, then give IV Ca first;
- limit protein intake w/ renal diet (organic acids);
- non dietary sources of a sudden increase in sodium intake include the administration of sodium bicarbonate or Shohl's solution in metabolic acidosis or the use of cation exchange resins for hyperkalemia;
- although the detrimental effects of acidosis on bones are esp manifested in children, they may be a cause of renal osteodystrophy in adults;
- administration of alkali therapy to minimize acidosis must, be weighed against the threat of volume overload;
- hyperchloremia acidosis is not typical of renal failure;
- its presence signals the existence of volume contraction;
- antacids may also bind Fe & limit absorption from intestine;
- harmful effects include nausea, vomit, & cerebral dysfunction, cardiac depression, insulin resistance, and impaired cellular metabolism;
- acidosis will also contribute to hyperkalemia;
- metabolic acidosis is treated w/ Shohl's solution, IV bicarbonate, or dialysis;
- Hyponatremia:
- although the capacity to dilute urine becomes severly limited only at very low GFRs, pts with renal insufficiency are prone to hyponatremia from water retension if given a fluid load;
- free water intake is exceeding free water elimination;
- this occurs when administration of IV fluids is excessive and hyptonic
- when hyponatremia begins to evolve, free water restriction must be prescribed;
- if the serum sodium concentration falls below 120 mEq per liter, convulsions are immenent;
- dialysis is the only maneuver that can correct the hyponatremia in this situation;
- administration of hypertonic NaCl in the oliguric patient with severe hyponatremia is prohibited, because patient is almost always fluid overloaded;
- HyperPhos:
- must be controlled as it promotes metastatic calcification and osteodystrophy; (keep Phos below < 5.0)
- decr phospate may prevent calcium precipitation in tubules;
- consider Phoslo or Amphogel;
- avoid Fleet's enema
- consider Ca acetate to bind phosphorous;
- use of phosphate binding gels should be monitored, especially if a patient is on a low protein diet that will decrease production of nonvolatile acids;
- combination may severely restrict the availability of urinary phosphate for titratable acid, and this could further limit net acid excretion;
- Renal diet:
- dietary objective is to maintain the pt at a wt which will keep blood pressure in good control and renal function stable;
- 4 gm salt diet will suffice for most patients;
- if the wt rises then further reduction is necessary;
- addition of lasix may permit a higher sodium diet;
- restrict Na gradually;
- diseased kidneys appear to waste salt, continuing to excrete Na to point of dehydration & vascular collapse when Na intake is suddenly restricted;
- when sodium intake is reduced gradually (4 to 14 wks), renal function can remain stable on a sodium intake as low as 5 mEq/day;
- if dietary sodium intake is suddenly curtailed, excretion of Na will continue, & negative sodium balance, w/ volume contraction, decreased renal perfusion, & further reduction in GFR;
- it is inappropriate to routinely restrict dietary sodium intake;
- Na restriction should be reserved for pts with evidence of total body sodium excess (CHF, Edema, HTN)