Protect those nephrons! From AMR this week, a handy primer on CKD for your continuity clinic.
When do your patients have CKD? Decline in GFR for >3 months PLUS Evidence of Kidney Disease (evidenced by one of the following)
- Urine sediment abnormalities
- Electrolyte and other abnormalities due to tubular disorders
- Abnormalities detected by histology
- Structural abnormalities detected by imaging
- History of kidney transplantation
Figure out what caused it: 75% are HTN and/or Diabetes
- Glomerular disease
- Obstructive uropathy
- Vascular diseases
- Hepatorenal/cardiorenal syndromes
- Congenital disease: PKD
Do the workup:
- GET THE UA Active sediment/proteinuria vs a bland UA will be a major branch point in your evaluation, so you have to get a UA. Spot urine protein and creatinine are also useful.
- US Looking for cystic kidneys, hydronephrosis, asymmetry, or even symmetric evidence of “medical renal disease” is useful.
- Based on historical clues, you can also check: HIV, hepatitis serologies, SPEP/UPEP, ANA, ANCAs
Stage it: based on GFR. VGFR- MDRD and CKD-EPI are most commonly used formulas. Here’s a handy calculator that gives you both, plus the stage.
||Kidney damage with nl GFR
||Kidney damage with increased GFR
||Moderately decreased GFR
||Severely decreased GFR
||<14 or on dialysis
Call for Backup: Nephrology Referral
- You don’t know why the patient has kidney disease
- It is progressing quickly (loss of 50% of their GFR within one year)
- Nephrosis: Lots of proteinuria (>3g/day)
- Nephritis: active urine sediment with blood, protein, casts
- Dialysis planning: sometime during stage3b is probably ideal, certainly by the time patient has GFR <30
- Mortality benefit for patients that see nephrology earlier.
OK, now what? Manage it:
- Fix reversible causes: remove nephrotoxins, relieve obstruction, treat CHF/Cirrhosis/HIV/Hepatitis
- Slow progression
- HTN: JNC8 guidelines recommend goal 140/90
- DM: ACCORD trial showed benefit with treatment to HbA1c <7.5
- Add an ACE-inhibitor or ARB if there is proteinuria
- Aggressive cardiovascular risk reduction (Cardiovascular disease is going to kill these patients before the renal disease does- see graph below)
- Deal with the complications
Sarnak M J et al. Circulation. 2003;108:2154-2169
- Hyperkalemia: Lasix helps
- Anemia: Replace Iron, consider EPO if Hgb <10
- Acidosis: consider when serum bicarb <22
- Volume Overload: Lasix helps
- Mineral Bone Disease: replace Vitamin D, bind PO4
Great posts by our own Dr.Centor on CKD here (don’t miss the comments) and here.
2012 KDIGO Guidelines for the evaluation and management of CKD.
Two cases of hyperkalemia in Red clinic this week uncovered a weakness in my own understanding of this issue. What to do? Write a blog post, of course.
Potassium balance occurs by moving potassium in and out of cells (thanks to all those pumps that you learned about in medical school) and regulating renal excretion of potassium (more pumps).
Hyperkalemia is due to either too much potassium released from cells or not enough potassium excreted by the kidney.
- Acidosis causes potassium to leave the intracellular space as H+ ions enter
- Hyperglycemia (DKA), it’s not so much the acidosis in this instance as it is the loss of intracelluar K due to osmotic forces from the hyperglycemia
- Tissue breakdown- seen most often in tumor lysis syndrome or trauma
To the kidneys
- Reduced aldosterone secretion: with nl underlying renal function, this is usually a small rise in K.
- Hyporeninemic hypoaldosteronism
- RX: NSAIDS, Calcineurin Inhibitors
- Acute glomerulonephritis
- Renal insufficiency- most common with diabetic nephropathy
- RX: Angiotensin system blockers (leads to rise in renin levels)
- RX: Heparin (usually chronic therapy) can be directly toxic to zona glomerulosa cells
- Adrenal Insufficiency (only primary AI, the pituitary is not a big regulator of aldosterone)
- Inherited disorders (that I am conveniently ignoring here)
- Reduced response to aldosterone
- RX: Potassium sparing diuretics (spironolactone), trimethoprim (1/2 of Bactrim)
- Pseudohypoaldosteronism Type 1 (another, albeit well named, congenital disorder that I am ignoring for now)
- Reduced distal sodium/water delivery (turns off the pumps): anything that decreases effective circulation volume, meaning that dehydration/hypovolemia AND hypervolemia in CHF or cirrhosis can be blamed.
- Key scenario here is the decompensated CHF patient with poor renal perfusion as they fall off the Starling curve, yet continue their ACE inhibitor and Aldactone.
- Acute or chronic kidney disease: typically it takes some renal hit (new or ongoing) plus one of the other things above to get truly clinically significant hyperkalemia. Key scenarios:
- The fasting dialysis patient. They are missing the insulin which helps maintain the potassium balance. This is why we give insulin and glucose IV when we keep ESRD patients NPO in the hospital.
- Late stage CKD patients who eat a high potassium diet. Most patients can eat all the bananas they want and not get hyperkalemia. Not so if your GFR is 20.
- Ureterojejunostomy (neobladder). The jejunum (that was used to make the bladder) absorbed potassium in a former life. Still does.
So how to make the diagnosis?
Think about the etiologies listed above. What fits for your patient? Look closely at medicines and renal function.
Is this an out of the blue hyperkalemia? Maybe it’s pseudohypokalemia/lab error- recheck.
If it is an acute rise (that you are pretty sure is real), think moving potassium out of cells. Tumor lysis syndrome? DKA? Acidosis?
If you are still stuck, look to the kidneys. Figure out if aldosterone is working correctly.
- Check Plasma Renin Activity (PRA), Plasma Aldosterone, and Plasma Cortisol. Ideally checked after patient is upright for 3 hours (not the time for the 8am cortisol value), or after being given a dose of lasix.
- Hyporeninemic Hypoaldosteronism- Type 4 RTA will have Low PRA, Low Aldosterone, normal cortisol
- Usually 50-70 yo diabetic patients with mild/moderate renal insufficiency
- Primary AI: low aldosterone, low cortisol. Nl or high PRA