Kidney Lecture

Question 1

Decrease in GFR causes what in your Cr levels?

Answer 1

Increase in serum Cr. It’s proportional to the GFR changes.

Question 2

GFR is equivalent to

Answer 2

Creatinine Clearence

= urinary Cr excretion/serum creatinine
= Urine creatinine * Volume urine / Serum Cr

Question 3

Cockroft-Gault Equation, which we don’t use as much but still can use in the clinic

Answer 3

CrCl = (140-age) * weight / (SCr * 72)

correction factor * 0.85 for females

Question 4

MDRD - CKD-EPI equations are better than Cockroft-Gault. What makes these guys better?

Answer 4

• Race correction factors included
• Don’t need weight
• More accurate for advanced kidney disease

Much more modern, better use of new age EMRs

Question 5

What causes uremia?

Answer 5

• Small protein-bound compounds, phenols, indoles, organic acids
• “middle molecules,” nitrogenous compounds with small molecular weight

uremia does not mean urea!

Question 6

Acute indications for dialysis

Answer 6

AEIOU

Acidosis
Electrolytes imbalances
Ingestions
Overload
Uremic Toxic syndrome

Question 7

What ingestions can cause an acute need for dialysis?

Answer 7

• Methanol
• Ethylene glycol
• Salicylates
• Lithium

Question 8

What overload can lead to an acute need for dialysis

Answer 8

Volume overload that can’t be fixed in normal medical ways

Question 9

What are uremic toxin symptoms?

Answer 9

• Serositis (pericarditis, pleuritis)
• Encephalopathy - Nausea/vomiting, mental status changes, seizures
• Bleeding (platelet dysfunction)

Question 10

What indicates a chronic need for dialysis?

Answer 10

• AEIOU

- GFR

Question 11

So who gets Acute kidney injury? (AKI)

Answer 11

• 1% of patients at time of admission
• 2-7% incidence during hospitalization
• 4 - 15% incidence post surgical

Question 12

What is the prognosis of those with acute kidney injury?

Answer 12

• 25-60% require acute dialysis
• 6% require long-term or permanent dialysis
• Associated with > 50% mortality

Question 13

So as you might expect, kidney injury can occur before the kidney, at the kidney, or after the kidney causing back up. What kind of injuries fall into these categories?

Answer 13

Pre renal azotemia
- Volume depletion (true hypovolemia, CHF, cirrhosis, sepsis)

Intrinsic renal injury

• Ischemic
• Nephrotoxic
• Immunologic (glomerular, vasculitis)

Post renal obstruction

• Bladder outlet
• Stones
• Extrinsic mass

Question 14

What causes acute tubular necrosis and what do we associate with it?

Answer 14

Often from prolonged pre-kidney azotemia (reduced blood flow and GFR without cellular damage)

Associated with volume depletion, heart/liver failure, post surgical, sepsis, nephrotoxic medications, pre-existing chronic kidney disease

ATN occurs when renal tubular epithelial cells are damaged either due to ischemic and/or toxic process

Question 15

So prerenal azotemia can lead to ATN. How do we distinguish the two in the clinic?

Answer 15

• Diagnosis by therapy - azotemia should resolve rapidly (hours) with restoration of perfusion pressure (volume repletion)
• UA - Azotemia usually has bland sediment, but ATN has isosthenuria and muddy brown casts

Question 16

So how many people get Chronic kidney disease and how does it present in GFR values?

Answer 16

About 20 million people in the U.S.

eGFR

Question 17

What defines the stages of Chronic Kidney disease?

Answer 17

Stage 1: eGFR >= 90
Stage 2: eGFR 60-89
Stage 3: eGFR 30-59
Stage 4/5: eGFR

Question 18

What are the leading causes of End Stage Renal Disease (ESRD) in the U.S.?

Answer 18

• Diabetes = 40%
• HTN = 20-30%
• Glomerulonephritis = 20%
• Polycystic Kidney Disease = 10%
• Others =

Question 19

Back to the stages we discussed earlier. What symptoms fall into these categories?

Stage 1: eGFR >= 90
Stage 2: eGFR 60-89
Stage 3: eGFR 30-59
Stage 4/5: eGFR

Answer 19

Stage 1: Hypertension, Hypervolemia
Stage 2: Same as 1
Stage 3: Hypertension and hypervolemia, as well as osteodystrophy, uremia and anemia
Stage 4: Same as 3, with Acidosis and hyperkalemia
Stage 5: Same as 4, just way worse in all categories and a GFR

Question 20

What is theory behind how/why kidney injury progresses to such a chronic state?

Answer 20

Theory: advanced CKD leads to further loss of functioning nephrons by a means independent of the original cause.
The remaining nephrons compensate through hyperfiltration, leading to glomerular hypertension and hypertrophy, then glomerular injury/scarring in the functioning nephrons. This sets up a vicious cycle leading to further reduction in nephron number.

Question 21

What does proteinuria tell us?

Answer 21

Abnormally high protein excretion is a hallmark of many forms of chronic kidney disease.

Proteinuria is probably not just a marker of kidney disease but also plays a role in the pathogenesis and progression.

Excessive tubular reabsorption of proteins in the proximal tubule may lead to activation of inflammatory, immunological, and fibrotic pathways causing further cell injury.

Proteinuria is a systemic marker of endothelial cell inflammation and associated with multi-organ morbidity

Question 22

How do ACE inhibitors help fight CKD?

Answer 22

Amelioration of glomerular hyperfiltration and hypertension (reduction of efferent arteriole resistance)

Reduction of proteinuria

Decreased angiotensin II production leading to possible decreased TGF-B effect

Question 23

What blood pressure targets do we shoot for in folks with proteinuria?

Answer 23

– Target:
With proteinuria = 140/90
Without = 130/80