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22 Cards in this Set

  • Front
  • Back

Proximal Tubule Function

Re absorbs 50% sodium (H+/NA+ exchange)


Reabsorbes bicarb


Absorbs all glucise and amino acids


PTH acts here to increase phosphate & Vit D reabsorption



Loop of Henle

40 % of sodium reabsorption


Main water reabsorption place


Loop diuretics block Na+/K+/2Cl- co transporter

Distal tubule

5 % sodium reabsorption


Thiazide diuretics 1st part - block Na/Cl cotransporter



Collecting duct

Spirinolactone blocks Na/K exchange


Lithium inhibits ADH

Nephrotic

>3..5g protein / 24h


Glomerular diseasea

CASTS


1) Tubular cells


2) Hyaline


3) Granular


4) Red Cell


5) Leukocytes

1) ATN / intestitial nephritis


2) Tamm-Horsfall glycoprotein (seen in N pop)


3) non-specific


4) glomerulonephritis or tubular bleeding


5) pyelonephritis or ATN

RTA vs renal failure on ABG

RTA - normal anion gap


renal failure - increased anion gap (excess amonia)

Type 1 RTA

Common


Distal


Impaired urinary acidification e.g. poor H+ excretion


Urine pH>5.3


Plasma HCO3- <10


Plasma K+ low


Complcations - nephrocalcinosis, calculi, poor growth, infections

Type 2 RTA

Proximal


Rare


Failure of HCO3- reabsorption


Bicarb 14-20


A.w osteomalacia, rickets, faconi syndrome

Faconi syndrome

Phosphaturia, glycosuria, aminoaciduria

CAuses of Type 1 RTA

Primary - genetic (AD) or idiopathic


Secondary to AI - SLE, sjogren


Tubulointerstitial - chronic pyelonephritis, transplant rejection, obstructive uropathy, chronic interstitial nephritis


Nephrocalcinosis - medullary sponge kidney, myeloma, amyloidosis


Drugs and toxins - lithium, amphotericin, toluene

Causes of Type 2

Idiopathic


With Fanconi - Wilson's, cystinosis, fructose intolerance, sjogren's


Tubulointerstitial - interstitial nephritis, myeloma, amyloidosis


Drugs and toxins: tetracyclins, lead, mercury, acetozolamide, sulfonamides

Type 4 RTA

mineral corticoid deficiency metabolic acidosis + hyperkalaemia.


Low renin low aldoseterone - DM, NSAIDS, Ciclosporin


low renin, low aldosterone: adrenal destruction, ACEi/ARB

Bartter

Like fruosemide - inactivation of Na/K/Cl transporter


Hypotension, hypokalaemia,


High levels of chloride in urine

Liddle's

Like Conns


Hypertension, hypokalaemia,


AD


low renin and aldosterone


No response to spirinolactone



Gitelman

Like thiazides


AR/AD


Hypocalciuria, hypomagnesaemia


Hypotension


Hypokalaemia


Later onset than Bartter

Stage 1 AKI


Stage 2 AKI


Stage 3 AKI

1) <0.5ml/lg/h >6hours. SCr increased by >26micromol/L or 1.5-1.9 x reference


2) <0.5ml/lg/h >12hours or >2.0-2.9 x reference SCr


3) <0.5ml/lg/h >24hours/anuria or >3x reference or >354 micromol

Minimal Change

Nephrotic


Children


NSAIDs/Gold


Tx: prednisolone

Membranous

Proteinuria, nephrotic (mild haematuria) may cause CKD


age - mid 20s or 60-70


IgG deposit in GBM


Tx ACEi ARB


May be secondary to malignancy, SLE, RA, Sjogren, chronic infections, drugs (gold, penicillamine, captopril, nsaids.)


Sarcoid, Guillan BArre, PBC.

FSGS

Protein ++, nephrotic a/w CKD & AKI.


Primary - Ig G deposits


secondary - due to HIV, heroin, obesity

Mesangioproliferative/IgA

Most common priamry GN in adults esp young men




AI


IgA component



Mesangiocapillary

Type 1 - immune deposits in subendothelial space. A/w cryoglobulinaemia, hep C.


Type 2: mesangiam deposits. Familial


Type 3: both and Hepb/c


Tx with steroids