16 - CKD/Kidney replacement therapy

Minimum amount of time kidney dysfunction has to be present for it to qualify as CKD

3 months

CKD definition

Either one of:

• Reduced GFR of 60 mL/min/1.73m²

• Signs/marker of kidney damage despite normal GFR

Best GFR markers

Exogenous: Inulin, radiotracers

Endogenous: Creatinine, cystatin C(If creatinine is distorted)

GFR relationship with creatinine

Inverse

What are examples of markers of chronic kidney damage?

• Persistent albuminuria/hematuria(2x samples over 3 months)

• Radiologic/pathologic findings

• History of kidney transplant

CKD classification system

CGA system:

• C (Cause). The underlying disease, such as diabetes, hypertension, glomerulonephritis, or polycystic kidney disease.

• G (GFR category), G1 to G5:

  • G1: 90 or more (normal or high)

  • G2: 60–89 (mildly decreased)

  • G3a: 45–59 (mildly to moderately decreased)

  • G3b: 30–44 (moderately to severely decreased)

  • G4: 15–29 (severely decreased)

  • G5: below 15 (kidney failure)

• A (Albuminuria category), A1 to A3:

  • A1: ACR below 30 mg/g (normal to mildly increased)

  • A2: 30–300 mg/g (moderately increased)

  • A3: above 300 mg/g (severely increased)

CKD early and late symptoms

Early: Nocturia

Late: Anemia with NCNC, renal osteodystrophy, decreased kidney size, dry skin

Most common causes of CKD

1. Diabetes mellitus

2. Hypertension

Stable vs progressive CKD

Stable CKD stops and works at a lower level, declining at the normal aging rate again. Meanwhile, progressive CKD continues to worsen after the original cause is controlled.

Progressive CKD mechanism

Surviving nephrons for loss of number by filtering more(Boosting GFR) via afferent arteriole dilation and constricting efferent arteriole(using RAAS) → Intraglomerular pressure rises which damages the glomeruli → vicious cycle

CKD complication framework

ABCDEF

A:

• Mechanism

• Treatment

• Anemia because damaged kidneys can’t release EPO to tell RBC precursors to mature → NCNC anemia

• Give iron if TSAT is 30% or less, synthetic EPO

B:

• Mechanism

• Treatment

• Blood volume and blood pressure is raised because damaged kidneys can’t filter out salt as efficiently, so water follows it back → edema, pulmonary edema, puffy eyes

• Salt restriction or drugs like ACEi/ARBs, Diuretics, SGLT2i, Finerenone

C:

• Mechanism

• Treatment

• CKD induced mineral and bone disorder because damaged kidneys can’t excrete phosphate or activate vitamin D → Ca2+ falls and PTH increases to release Ca2+ from bone → renal osteodystrophy

• Lower phosphate, vitamin D

D:

• Mechanism

• Treatment

• Keep sodium less than 2g a day, make sure protein isn’t too high(but also not too low, especially in dialysis patients)

E:

• Mechanism

• Treatment

• Kidney damage makes it so that less K+ is excreted, and when combined with things like ACEi/ARB/MRA, it can cause hyperK+

  • Treat w IV Ca2+ gluconate, insulin w glucose, then remove K+

• Metabolic acidosis: Ammonia productions slows down → acid accumulates

  • Oral Na+ bicarb.

F:

• Mechanism

• Treatment

• Unintentional weight loss, weakness, exhaustion, slow walking speed, physical activity all from sarcopenia caused by anemia, protein-energy wasting, weakened bone, etc

Sick day rule

Stop ACEi/ARB, diuretics, etc. during sicknesses like vomiting, diarrhea, dehydration

4 main protective drugs for the kidney

RAAS blockers, SGLTi for all patients + Finerenone + GLP1-Ra for DM2 patients

Why are RAAS blockers helpful in CKD patients?

• Best CKD indication

• Angiotensin II causes vasoconstriction, specifically so at the efferent arteriole which boosts intraglomerular pressure(GFR up) and also boosts aldosterone which retains sodium and brings back more volume

• RAAS blockers lower intraglomerular pressure and reduces albumin leak

  • CKD with A2-A3

Why is increased Cr after giving RAAS blockers okay?

It’s okay because we are reducing intraglomerular pressure, so less GFR will expectedly cause more sCr, but just not more than 30%

Why are SGLT2i helpful in CKD patients?

• Best CKD indication

SGLT2 normally reabsorbs Na+ and glucose(90%) at the PT, so inhibiting them allows the body to keep Na+ and glucose in tubules. This leads to more NaCl at the Macula Densa, thinking we have too much pressure, so it will constrict the afferent arterial and reduce intraglomerular pressure

• CKD pt. with eGFR above 20

Why are NS-MRA helpful in CKD patients?

• Best CKD indication

NS-MRA, or finererone, has two effects. One is reabsorbing less Na+, so less water follows and reduces blood pressure, but it also blocks aldosterone’s fibrotic and inflammatory triggering effect on podocytes, mesangium

• DM2 CKD with K+ not more than 5

Why are GLP1-RA helpful in CKD patients?

• Best CKD indication

GLP1-RA help with DM and weight loss by acting like insulin, slowing gastric emptying time and inhibiting glucagon, and helps in CKD albeit less clearly defined mechanism

• DM2 CKD

4 Final options to treat CKD

• When do we consider these options

Consider in stage 5 CKD(eGFR <15)

• Kidney transplantation

• Hemodialysis

• Peritoneal Dialysis

• Conservative Kidney Management