Neet PG Medicine Notes 2 – Renal System 2 – Renal Physiology


Ultrafiltration pressure

Difference between the two pressure

  • Glomerular pressure
  • Bowman’s space also called interstitium

Glomerular has two pressure  glomerular capillary hydrostatic pressure – oncotic pressure

Bowman’s space has two pressure

  • Interstitial hydrostatic pressure
  • Capillary hydrostatic pressure  60 mmHg

oncotic pressure 32 mm Hg

Interstitial hydrostatic pressure 18 mm Hg

60-32-18 = 10 mm Hg = net ultrafiltration pressure


Depends on

  • Core size
  • Permeability-surface area

12.5 ml/min/mmHg

Gfr = 10×12.5

Mesangial cell contraction produce

Surface area reduces and decreases GFR

How to measure GFR

Gold standard should be

  • Freely filtered
  • Not reabsorbed
  • Not secreted

Ideal molecule to measure GFR is inulin (gold standard)

The most sensitive and specific method to measure GFR Technicium EDTA clearance not used much

For all practical purpose, we use creatinine


  • 113 kDa
  • Produced in the muscle
  • The basic precursor is creatine
  • Clearance of creatinine is almost equal to GFR

Clearance of any molecule is UxV/P

Ucreat x flow rate of urine (ml/min)

P creat

Creatinn=ienundergoes tubular secretion

Creatinine clearnace= GFR + tubular secretion

Creatinine clearance always overestimates GFR


Urea clearance = GFR – tubular secretion

Urea clearance underestimates GFR

We still using creatinine is used as bedside marker for GFR

23-year-OLD BOY who weighs 72 kg with serum creatinine is 1.2

60 yr old female who weighs 42 kg and her serum creatinine is 1.2

Cr CL  is calculated by Cockroft and Gault equation =

(140- age) x body weight

72 x S. creatinine

For female

(140- age) x bodyweight x 0.85

72 x S. creatinine

For the boy = 100 ml – normal

For the female = 80x 2/3 x 2/3 =320/9 = 40 ml/min – big issue

So this same creatinine clearance for a young person may not be correct for an adult

For a diabetic for 10 years with creatinine report of 1.5 and weight 48 kg



80×2  = 160/4.5 = 1600/45 = 36 ml/mt


In a patient with diabetic nephropathy serum creatinine is 1.2 one day next day 1.5

Another patient serum creatinine is 60mg/ml one day next day 12 mg/ml

Which Is more significant

First patient gfr dropped from 66 to 53

For second patient drop from 13 to 7

For the patient, if creatinine is 6 or 7 or 8 it is not much problem but when it is 1 or 2 or 3 then it is more significant

Pitfall in creatinine

  • Fails to rise soon after injury LIKE DRUG INDUCED
  • Near normal in CKD
  • More muscle mass more clearance
  • Drugs which compete with creatinine cimetidine and trimethoprim compete for tubular secretion and increase creatinine
  • Sex male more muscle mass

The only marker close to creatinine is cystatin C

Cystatin c

  • Produced by nucleated cell at a constant rate
  • The problem was elevated nonspecifically in inflammation and hypothyroidism

The best method for creatinine Cocroft and Gault equation

Problem with this equation

  • Method of creatinine estimation
  • This equation was done when the estimation was done by Jaffe’s method or alkaline picrate or colorimetric
  • Now we are using standardized assays such as spectroscopy and the equation does not properly fit into this assay

Cr Cl is not always = to GFR it always overestimates

It gives importance to body weight

Currently used method for Gfr

CKD – epi equation (epidemiology problem initiative)and mdrd equation (modification of diet in renal disease)

CKD-EPI  is the best method

Why we prefer CKD-EPI

  • Higher levels of GFR is right at a low level both are best
  • Renal autoregulation
  • Mean BP is as high as 180 and as low as 80 Blood flow to the kidney is constant

Renal blood flow is 1200 ml/min

Renal plasma flow is 700 ml/min

Molecule you use to estimate plasma flow is para amino hippuric acid

Renal autoregulation is depended upon two structure – Afferent arteriole and efferent arteriole

If afferent arteriole dilate is the best for kidney and increase GFR

Efferent arteriole constrict also increase GFR

Afferent arteriole controlled by prostaglandin PGE2 and PGI 2

Efferent arteriolar constrict controlled by angiotensin 2

Afferent arteriolar is preferred to efferent constriction

Because no blood into the medulla and kidney will go for hypoxia

We don’t want efferent arteriolar constriction

For back pain taking NSAID for 23 and 60 years old

For 23 it is momentary constriction of efferent arteriole because at that age they have angiotensin 2

But for 60 angiotensins 2 is less he is surviving purely by an efferent arteriole

But now NSAID shuts his efferent arteriole and afferent arteriole is already not functioning so no maintainenece fo GFR and kidney goes for shut down

Renal autoregulation is maintained by two things

  • Myogenic reflux
  • Tubuloglomerular feedback

Both are same but in Tubuloglomerular feedback we have a molecule called adenosine but Myogenic reflux  is a stretch reflex

 See the diagram to understand to what happens in dilation and constriction of efferent and afferent arterioles

ACE inhibitors are contraindicated in bilateral RAS

For a patient with bilateral RAS the afferent arterioles are constricted and the function is taken over by efferent arteriole dilation so for this patient, if we give NSAID it will block the angiotensin and efferent arteriole also goes for constriction and total renal shutdown so ACE inhibitors are contraindicated

Sympathetic endothelin and histamine decrease the GFR

Dopamine prostaglandins nitric oxide atrial natriuretic factor and bradykinin will increase GFR

The endothelium is acted by two receptors

  • ETA receptors – vasoconstrictor of the afferent arteriole
  • ETB receptors – promotes natriuresis it is good for kidney

Tubuloglomerular feedback

Glomerular tubular balance

Today my gfr is 100ml/mt

100meq of sodium are filtered and 99 meq are reabsorbed and  1 meq is excreted

Tomorrow my gfr is 200 ml/min so 200 meq of sodium is filtered and 198 meq is reabsorbed and 2 meq is excreted which means the percentage of reabsorption is the same in the sense percentage of solute excretion is always the same and has nothing to do with renal autoregulation.

Filteration fraction

FF = GFR/renal plasma flow

     = 125/700 = 0.1-0.2 =FF

INCREASE ff increase proximal tubular reabsorption

Out of RPF how much GFR is there is FF

When filtration fraction increases – plasma concentration of plasma in peritubular capillary increases – increase oncotic pressure – decrease in renal interstitial pressure- more reabsorption across proximal tubules

Countercurrent multiplication system

Serum osmolality is 285-290 mmol/kg of H2O

Urine also will have an osmolality of 285-290 mosmo so at the PCT the urine has an osmolality of 285-290l

When the fluid is coming thru the thin descending loop of Henle only water is reabsorbed by the time it reaches the tip the osmol increase to 1200 mmolosmol of water

Fluid leaving the PCT is iso-osmolar

This phenomenon is called countercurrent multiplication that is the increase from 290 to 1200 milliosmol /kg of water

Countercurrent exchange

Our normal urine osmolality is 700-800 mosmol/kg of water

Urine is far more concentrated than blood

Excreting concentrated urine  how

In ascending limb the solute is permeable by the time it reaches distal convoluted tubule the osmolality becomes 100

From 100 how it becomes 700 this increase is done by vasopressin or ADH

ADH acts with the help of receptor V2 receptor

There are two V2 receptors

  • AQP3
  • AQP4

This V2 receptor will increase your cyclic AMP and also protein kinase A

Protein kinase A increase the aquaporin  AQP2 with this help lot of water will reabsorb that is the reason why the osmolality increases form 100 -700

 high medullary interstitial osmolarity

the third player is urea reabsorbed from IMCD(medullary interstitium)

urea is not lost because the descending limb will take in urea and the ascending limb will give out urea

vasa recta

this whole phenomenon in countercurrent exchange

in a nutshell, the four thing needed for countercurrent exchange is

  • ADH
  • High medullary interstitial osmolarity
  • Urea
  • Vasa recta

Which among frusemide and thiazide will produce more hyponatremia

Frusemide – Na+-K+-2Cl- – low medullary osmolality

Thiazide – Na+ – Cl- – maintains medullary osmolality – ADH acts – hyponatremia so thiazide produce more hyponatremia

























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