Hyperphosphatemia, Hypocalcemia and Hypermagnesemia.
Decreased production of 1,25-dihydroxy vitamin D3 results in decrease GI Ca ++ absorption.
Decreased ability of the kidney to excrete PO 4 - .
These result in a decrease in serum Ca ++ which leads to an increase in PTH which results in increased bone reabsorbtion of Ca ++ in an attempt to normalize free Ca ++ levels and leads to renal bone disease.
Gradual decrease in tubular handling of K + can result in hyperkalemia.
Usually occurs when GFR severely reduced (<10 ml/min).
K + restriction often needed.
Diabetics with Type IV RTA / Hyporeninemic Hypoaldosteroneism can develop hyperkalemia without a severely depressed GFR.
Stop replcmnt Excessive Ca/VitD replcmnt ↓ variable ↑ Phos binders and Vit D Severe 2 º hyperPTH ↑↑↑ ↑ ↓ Phos Binders 2 º hyperPTH ↑ ↑ ↓ 1,25 OH Vit D Vit D def ↑ ↓ ↓ Treatment Process PTH Phos Calcium
So my pt presents with concerning Hx and PE. What studies to do I need??
K+, Creatinine, Ca++, Mg, Phos
Small kidneys bilaterally
But don’t forget !!
Renally dose medications such as antibiotics/antiretrovirals, ranitidine, atenolol
Be extremely cautious with starting an ACEI or ARB. Talk with consultant.
Avoid using Morphine as toxic metabolites build up.
If diuresis is necessary, use lasix if patient has hyponatremia, and thiazide if pt has hypernatremia
However, thiazides are not effective when GFR <30
Causes of Chronic Renal Failure
Urinary tract pathology
Idiopathic Membranous Glomerulonephritis.
Focal and Segmental Glomerulonephritis (FSGS)
Associated with HIV
IgA Nephropathy (Berger’s Disease).
Membranoproliferative Glomerulonephritis Type I and II (MPGN I and II).