What are the functions of kidney?

Endocrine : Secretion of renin and erythropoietin. Production and metabolism of PGs and kinins.

Metabolic: Activation of D3, gluconeogenesis, metabolism of insulin, drugs and CYP 450 activation.

GFR is the amount of plasma that if filtered through glomerular into the bowman's capsule and also relates to drug elimination. It is the best indicator of the kidney function.

The normal range is 120ml/min/1.73 (normalized BSA)

Pre-renal/functional: Pre-renal azetemia is the pre-renal hypoperfusion such as bleeding or thirst and drop in effective circulation volume from CHF. So the kideny will hold onto Na, K and urea. Pre-renal azitemia is temporary. Functional is more drug induced.

Acture Instrinsic: Include glomerular nephrosis, tubular damage, and acute interstitial nephritis. May cause CKD after and mostly it happens.

Post-renal: Obstruction of the outflow of the urine due to obstruction such as kidney stones.

For assessment talk about Scr and what you know about it?

How made, eliminated, and normal range?

How is it a good marker?

Creatinine is made from muscle mass. It is eliminated by eliminatin and secretion in the kidney. The normal range is .96mg/dL for women and 1.16 mg/dL for men. If the Scr goes up then it means there is something wrong, and it indicates that there is something wrong with the kidney fuction.

But also higher levels of Scr can be seen in body builders, after a steak dinner. Similarly, low levels can be seen in vegetarians, malnutritioned, and people with hepatic issues.

What are the albuminuria? What are the types, indicators and the values?

Albuminuria is presence of albumin in urine and it is an indication of poor glomerular filteration. The albuminurea is three types.

Normal: less than 30.

Microalbuminuria is 30-299 and Macro is greater than 300.

Everyone with CKD should be checked for albuminuria on regular bassis. To be sure of micro or macro albuminuria, 2 out of 3 tests have to be positive with 3-6 month time period.

What are values of Urine sodium Concentration and Urine osmolality?

What assessment can be made based on urine output?

Pre-renal Na is less then 20mEq/L and osmolality is more than 500.

Pre-renal: Na is more than 40mEq/L and less than 350-400.

Normal value is 500-2000ml/day. oliguria is less than 500ml/day. Less is 100ml/day is a huge issue.

Rules of thumb and limitations for C-G equation?

IBW= 50kg+2.3kg for each inch over 60 (males)

45.5kg+2.3kg for each inch over 60(females)

If height not available, use ABW.

If ABW is <IBW then use IBW.

If obese > 30% of IBW, then do the dosing weight .

Calculate using (IBW-ABW)(.3)+(IBW)

If the Scr is less than 0.8 then adjust it to 0.8

Only used in adults with stable kidney function, not adequate been used in females, elderly, or obese.

Also, issues for people less than 5 feet tall.

Criteria 1. You have structural damage for more than 3 months. Such as detection of albuminuria for more than 3 months.

Criteria 2. If you have GFR <60 for over 3 months.

1. Not a stage but at risk population. No evidence of damage by GFR of atleast 60 or higher.

2. Stage 1, the GFR is >90 but have renal damage.

3. Stage 2, GFR is between 60-90 but have apparent damage to the kidney.

4. Stage 3, the GFR is between 30-60. You almost lose 50% of you kidney mass.Slowing the progression is the only option, no reversing.

5. Stage 4, the GFR is 15-29.Most likely will go on dialysis.

6. Stage 5, GFR is less than 15%. Need renal replacement therapy.

Diabetes (most)

Hypertension (second most)

Glomerularnephritis (long standing UTIs can cause that too)

Cystic kidney (genetic disorder, develops in adulthood; later in life)

Insult kidney, one nephron dies and other start working twice as much. Eventually they give up on you as well.The afferent arteriole dilates and efferent constricts. Capillary endo and epithelials dysfunction, and the filteration barrier breaksdown. The proteinuria, sends cytokines which leads to infilteration of inflammatory cells and golmerular and tubulorinterstitial fibrotic scarring causes damage.

The solute balance is maintained through an

a. Increase in GFR of remaining nephrons

b. Increase in secretion

c. Decrease in reabsorption

The goal for BP for CKD is less than 130/80 all the time.

Also, if the patient has diabetes or proteinuria, used ACE-i and ARBs for CKD.

Plus, the pt may need an additional 2-3 drugs to get BP to goal.

Use diuretics, loop if less GFR<30. May also need some Ca channel blocker. Treat micro or macro albuminuria by using ACEi or ARB.

Increase total body Na and H₂O level, causes HTN and edema.

If the pt has stage 3 CKD, GFR of 30-60. It decreases the ability to concentrate the urine at night cause nacturia.

At stage 4, GFR 15-29, the ability to withstand changes in Na and H₂O decreases. Any changes will cause hyper or hypo natremia and edema

Peripheral edema: Water accumulation in peripheries, and measured by using pit depth and count by using 1+ to 4+.

Anasarca: Total body edema. Water accumulates in the entire body.

Pulmonary edema: Life threatening, needs to be resolved immediately.

At GFR <60ml/min, the possibility of anemia increases and annual exam needs to done.

The outcomes with anemia heart failure, right ventricular hypertrophy, Increased hospitalization and mortality, and decreased quality of life.

Symptoms: Poor health, decreased sexual activity, cold intolerance, fatigue, mental sluggishness, and shortness of breath. 

Primary cause is erthropoietin.

Iron deficiency, uremia, decrease in blood, decreases life span of RBCs, vitamin B12 and folate deficiency.

Oral iron repletion which is cheaper but can cause side effects of being harsh on GI, poor absorption and chances to have the drug interactions. Recommended dose is 200mg in doses throughout the day.

IV iron repletion

1. Na Ferric gluconate, HD 125 mg X8HD sessions.

2. Iron sucrose. HD 100 mg X5HD sessions, ND-200mg X5 doses in 14 days. PD-300mg X5 doses, 14 days.

3. Ferumoxytol-HD, PD and ND use 500mg IV and another 500mg IV 3-8 days.

Erythropoietin stimulating agents are glycoprotein made either recombinant DNA or

Epogen-HD, PD and ND, Recombinant human and hurts during subcut so decrease conc by 15-30%.

Darbepoeitin; used in HD, PD and ND. admins q4weeks and can cause RBC aplasia.

Peginesatide: HD IV route and PD subcut route. once monthly and no results of red blood cell aplasia.

When to consider ESA therapy in patients on HD, PD and ND?

What are the goals for ESA therapy?

In HD and PD when the Hgb <10

In ND-CKD use when Hgb <10, meet criteria for transfusion to reducing the risk for transfusion.

 In HD and PD if the Hgb>10 start thinking about starting or lowering the dose.

In ND-CKD if Hgb>11 start reducing or stopping ESA therapy.

Describe the abnormalities with phosphorus.How does it lead to MBD-CKD

The Phosphorus filteration decrease, PTH activates to decreases reabsorption of Phosphate but at stage 5 can't do it. That leads to hyperphosphatemia, SHPT and hypocalcemia as the GI reabsorption of Ca has decreased.

 The SHPT mobilizes and increase resorption calcium and causes osteitis fibrosa cystica.

If high calcium and low PTH don't use the following. Elemental Ca max is 1500 or 200 with binders.

Calcium carbonate. 1-2 tablets with meal or snack and calcium acetate. 2 cap with meal or snack.

With high calcium and low PTH use

1. Sevelamer carbonate, dosing based on PO4 levels and usually 800-1600mg.

Lanthanum carbonate with usual dose of 500-750mg with food or snack.

What is the treatment for low vitamin D-CKD?

What are the calcium activated drugs are available and what are the doses?

For low vitamin D-CKD first measure the amount of Vit D.

If low <30ng/ml, then replete with cholecalciferol (D3)or ergocalciferal (D2). Also, using 25-OHD may to have beneficial effects seperate from 1,25 dihydroxy vitaminD.

1. Calciterol; daily or TIW (Vitamin D3)

2. Percalcitol daily or TIW (vitamin D2)

3. Doxecalciferol; daily or TIW (Pro-drug D2)

The decrease can occur due to drug-drug interaction, neuropathy, gastropathy (increasing transit time), N/V, higher gastric pH, 

The increase can occur due to decrease in first pass metabolism and decrease in p-glycoproteins in intestines.

Alteration in protein binding. (1)Low albumin, leaves more drug to interact with other tissues. (2)Free uremic by products or drug metabolites compete for binding sites on the protein.(3) the binding sites of the albumin are altered. For example, digoxin Vd decreases due to competition with uremic biproducts at the myocardium site and increases serum levels.

Hypoalbuminemia regardless of CKD;

reported total/(0.2*albumin)+0.1

Hypoalbuminemia plus CKD stage 4 or 5:

reported total/(0.1-0.15*albumin)+0.1

if ESRD & CrCl <10ml/min used 0.1 and for 10-24 ml/min use .15

Scr>12 and Bun>100

intractable nausea/vomiting

Uremic pericarditis

Fluid overload/CHF

Pruritis

Uremic Encephalopath or neuropathy

Myoclonus