Outpatient / Nephrology
Chronic Kidney Disease (CKD)
# Stage *** Chronic Kidney Disease 2/2 ***
G1 (>90) / G2 (60-90) / G3a (45-60) / G3b (30-45) / G4 (15-30) / G5 (<15 or on dialysis)
Intake:
-- GFR Trend: ***
-- Symptoms: *** fatigue, n/v, anorexia, pruritis, AMS, peripheral neuropathy, bleeding, edema, dyspnea
-- Red Flags: *** sudden drop, overload, AMS c/f uremia, bleeding, electrolyte imbalance
-- Meds: *** NSAIDs, acyclovir, PPI, ACE/ARB, diuretics, bactim, etc.
-- Etiology DDx: *** diabetes (47%), HTN (28%), glomerular disease (7%), cystic kidneys (3%), other - polycystic kidney disease, NSAID use, amyloid, idiopathic (15%)
Plan:
Workup
-- Initial Diagnosis: *** repeat creatinine and send Cystatin C to confirm a consistent decrease in GFR over a 3 month period; Labs - CBC, calcium, phos, A1c, urinalysis, Albumin:Cr, Protein:Cr, PTH, VitD, iron studies, HCV; Imaging - renal ultrasound
-- Monitoring: *** q4-12 month creatinine and BMP; Annual CBC, Albumin:Cr and Protein:Cr ratios, PTH, VitD, iron studies
-- Refer to Renal: *** GFR <30-45, acute decrease in GFR, Alb:Cr >300, resistant HTN
Treatment
-- BP Control: *** (goal <130/80; ACE/ARB best, then CCB, then thiazide if GFR >30)
-- Proteinuria: *** (goal <300mg/d; if higher add ACE/ARB)
-- Diabetes: *** (Goal A1c ~7%, metformin, SGLT2i if GFR >45, GLP-1 if GFR >30, insulin any GFR)
-- Statin: *** (all >50yo, diabetes, ASCVD risk >10%; dose reduce GFR <60)
-- Anemia/Iron: *** (Goal Hgb 10-11.5, replete when Tsat <30% and ferritin <500; IV preferred; consider EPO if Hgb <10 despite repletion)
-- Acidosis: *** (goal HCO3 >22; Sodium Bicarb 650-1300mg TID)
-- Bone Health: *** (If PTH elevated >2x ULN; goal phos <5.5 - restrict phos in diet, add sevelamer 800mg TID with meals; if on dialysis, supplement with calcium and vitamin D)
-- Nutrition: *** (Nephrocaps, fluid restrict PRN with sodium restriction <2g/day if edema)
-- Lifestyle: *** exercise, smoking cessation
-- Avoid NSAIDs, PPI, contrasted studies, blood draws in non-dominant arm; renally dose meds
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Patient Guidance and Information
New Diagnosis of CKD
Based on your lab results, you have chronic kidney disease, which means your kidneys are not working at full capacity. This may be in part due to ***
Kidneys are important for filtering out toxins from our body and keeping an appropriate balance on fluids and electrolytes. As such, we wil periodically keep an eye on many of these levels, at least once per year.
The best ways to prevent worsening of kidney function include controlling blood pressure, diabetes, losing weight, stopping smoking, and avoiding medications that can damage the kidney like ibuprofen/naproxen (Advil/Aleve).
If You Remember Nothing Else
Chronic kidney disease (CKD) is either abnormal renal anatomy or function for >3 months and is commonly caused by HTN and diabetes. Kidneys are able to work at near normal capacity with very little reserve, thus patients often only present with symptoms and sequelae (including fluid overload, uremia, anemia, hyperkalemia, hyperphosphatemia, and acidosis) late in the course. Medications shown to help prevent the progression of CK D include ACE/ARBs and SGLT2 inhibitors. Other management is based on treating co-morbidities and managing the downstream effects of CKD. While CKD can be managed by primary care physicians, when the GFR is less than 30-45, there is an acute decrease in GFR or the Albumin:Creatinine ratio is >300, involving renal consultants for management and discussions of renal replacement therapy or transplant is likely warranted. Early referral is important because it takes around 6 months to prep for dialysis in the non-acute setting.
Clinical Pearls
- CKD is defined by GFR <60 OR kidney damage (albuminuria >30mg/d); calling it ESRD implies you need to have RRT
- When to Refer: GFR <30-45, rapid decrease in GFR, albumin:Cr >300, resistant HTN, PTH >1000, hereditary kidney disease
- Urinalysis detects albumin but no other proteins - albumin is an independent predictor of mortality and CKD progression
- Cystatin C is a measurement of GFR that does not account for muscle mass and adds accuracy
- Can develop complications at the following GFR - hyperPTH (50), anemia (44), acidosis (40), hyperK (39), hyperPhos (37)
- It takes at least 6 months to prep for dialysis (in a non-acute setting)
- Dialysis Access Options: double-lumen central catheter (tunneled or temporary, infection); AV graft (maturation time but thrombosis & long-term complications); AV fistula (infection, overall mortality vs. catheters/AVG, but 6+ week maturation time + 50% primary failure rate)
- Fistula - “arterializes” the vein - makes the wall thicker; we do this because veins are easier to access so you can cannulize it well; note that a graft is foreign material
- Renal Transplant has mortality and QOL benefit over dialysis and is more cost effective; patients should undergo workup when GFR <30, and can be listed when GFR <20 - ideally get the transplant before HD start if possible; Contraindications to Transplant: short life expectancy, active malignancy, substance use disorder, concern for challenges with nonadherence to immunosuppressants; note that age/HIV/psych comorbidities are NOT contraindications
- Cyclosporine and tacrolimus (calcineurin inhibitors) can cause AKI, but over time are nephrotoxic due to chronic fibrosis
- Once you are on dialysis, creatinine levels become useless
- Urine output is the best way to see what the renal residual function is - we usually make 1-2L of urine per day with healthy kidneys, you can still make this amount of urine with ~5% of kidney function; one way to see if residual renal function is dropping on dialysis is to see if the phos is going up
- We often give diuretics like torsemide to keep the kidneys making urine; if you dose 200mg IV lasix and they don’t put out, they probably aren’t going to make urine
- Diabetic nephropathy leads to nonenzymatic glycation of proteins which leads to hypertrophy and proliferation of mesangial cells, GBM thickening, and characteristic nodular glomerulosclerosis
- Hypertension causes damage to vasculature at high levels, but at lower levels due to autoregulatory vasoconstriction of preglomerular vessels which can lead to decreased perfusion and ischemic damage
- Kidney’s endocrine activity is via hydroxylation of calcifediol to calcitriol (active form) - decreased VitD in CKD - this in combo with increased phosphate leads to decreased serum calcium and increased PTH
- Secondary hyperPTH from CKD is due to decreased Phos excretion that leads to decreased serum calcium, together leading to increased PTH secretion to try to tell kidneys to get rid of Phos and take calcium from bone
- Tertiary hyperPTH due to longstanding secondary hyperPTH that leads to gland hyperplasia
Trials and Literature
- CKD in the General Population Statistics
- Race in GFR leads to underdiagnosis, referrals, and transplant in black patients
- ESRD is 3.8x more prevalent in black patients
- VA NEPHRON-D Trial - Don’t treat with both ACE and ARB - one or the other - NEJM 2013; treating with both increases the risk of hyperkalemia and AKI but does not change renal outcomes (time to decline in GFR >30)
- MDRD Study - very low protein diet did not delay progression to kidney failure or all-cause mortality in those with stage 4 CKD, actually increased risk of death
- CHOIR Trial - NEJM 2006 - if use EPO, the target Hgb should be ~11, if target Hgb >13.5, increases the risk of death and hospitalizations
- CORAL Trial - NEJM 2014 - renal artey stenting along with medical treatment does not improve renal or cardiac outcomes in pts with hypertension or CKD 2/2 renal artery stenosis activation vs just medical treatment alone
- IDEAL Trial - NEJM 2010 - in pts with stage 5 CKD, there is no difference in survival or outcomes in early (GFR 10-14) vs late (GFR 5-7) initiation of dialysis; however most in the late arm got it earlier (around GFR of 10) due to uremia; this trial overall supports the practice of dialysis in symptomatic patients (regardless of GFR) or asx patients with GFR ~10 or less
Other Resources
- Clinical Problem Solvers: CPS CKD Schema
- MD Calc: Tangri Risk Score - the risk of developing Kidney failure requiring dialysis over 2 and 5 years
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