You are on page 1of 77

The Wolf Boy

• a childe that was carried away in the

Forest of Ardenne by Wolves, and
nourished by them. This child having
conversed with them divers years, was at
last apprehended, but could neither speak
nor walk upright, nor eat any thing except
raw flesh, till by a new education among
other children, his bestial nature was quite
Renal Failure

Zhao Mingyao
Functions of kidney

renal failure?

renal failure
Regulation Homeostasis
Endocrine disorder
Three types of RF
Nephron damage

ARF End stage


Body self
CRF intoxication

Intact nephron loss

Part 1 basic pathological taches
for renal failure
1. Dysfunction of GF:
blood flow, pressure, filtration, permeability of filtration
2. Renal tubular Dysfunction:
proximal, henle`s loop, distal tubule
3. Renal endocrine dysfunction:
RAAS, EPO, active vitamin D, Kallikrein-kinin-
prostaglandin-system, PTH, gastrin
Part 2 Acute renal failure
• Sudden and severe decrease in kidney
function that is short term.
Section 1 etiology and



Causes of ARF in hospitalized pts
• 45% ATN
Ischemia, Nephrotoxins
• 21% Prerenal
CHF, volume depletion, sepsis
• 10% Urinary obstruction
• 4% Glomerulonephritis or vasculitis
• 2% AIN( acuteinterstitial nephritis )
• 1% Atheroemboli
classification of ARF
1.urinary volume
oliguric ~
2. structure states
3.Damaged site
Section 2 pathogenesis o f ARF
1.renal hemodynamic alteration
(1)renal perfusion pressure ↓
(2)renal vasoconstriction
(3)renal vascular endothelial swelling
(4)intrarenal DIC
2.renal glomerular injury
renal glomerular injury
3.renal tubular injury

(1) renal tubular occlusion: cast obstruction,

interstitial edema
(2) Back-leakage of the glomerular filtration
urine backflow
(3) tubulo-glomerular feedback (TGF)
[Na+] macula densa( Juxtaglomerular
Apparatus ) afferent A GFR
4. Renal cell injury and its
• ( 1) cell injury
tubular cell
vascular endothelia
(2) Mechanism of cell damage
• 1) ATP and ion pump
• 2)OFR
• 3)glutothine
• 4)phospholipase
• 5)cytoskeletal structure
• 6)neautrophil and inflammation
• 7)apoptosis
What are these?
Section 3 alteration of
metabolism and function
• Three stages
• Oliguric ~ 75% of mortality

• Polyuric ~ 25% of mortality

• Recovery ~
1.Oliguric stage
• (1) urinary alteration
volume: oliguria and anuria
specific gravity: hyposthenuria and
component: Na+, Pro, cell debris, cast
(2)water intoxication

• Endogenous Water
• Water intake
• Renal excretion
(3) hyperkalemia

• Excreting K
• [K+]c release
• Acidosis
• Hyponatremia: Na+-K+↓
• K+ origin: storage blood, food
( 4 ) metabolic acidosis
• Excreting H+, NH3 and reabsorbing
• Catabolism
• BUN 10~15mg%
• NPN > normal level
Brief summary
• (1) urinary alteration
• (2) water intoxication
• (3) hyperkalemia
• (4) metabolic acidosis
• (5) azotemia
2.Polyuric stage
Mechanism of polyuria
1. reperfusion of damaged nephron
2. tubular obstruction released : Interstitial
edema faded and casts rushed out
3. the function of neonatalrenal tubule is
4.osmotic diuresis of urea
3. Recovery stage
• Most normal
• Tubular function recovery in end
• Few convert CRF
Why does not urinary volume
decrease in some ARF?
Comparison between normal person and nonoliguria RF

plasma filtration L /d reabsorption % end urine/d

Normal 180 99 1.8

Nonoliguria 90 98 1.8

9 80 1.8
Section 4 Prevention and
• Treatment of primary disease
• Protect nephrons
• Treatment according to symptoms
• dialysis
Part 3 chronic renal failure(CRF)
Section 1 etiology and clinical
• Chronic renal failure and ESRD affect more than
2 out of 1,000 people in the U.S.
• Diabetes and hypertension (high blood pressure)
are the two most common causes and account
for approximately two-thirds of the cases of
CRF. Other major causes include the following:
• Glomerulonephritis of any type (one of the
most common causes)
• Polycystic kidney disease
1.Etiology of CRF
(2)intrarenal: chronic
glomerulonephritis(50~60%) before;
diabetic nephropathy and hypertensive
2. Clinical courses
(1) silent (compensatory):GFR
(2)renal insufficiency: GFR25 ~50 /min
(3) renal failure:GFR5 ~25 /min
(4)end stage renal failure (uremia):GFR
<5 /min
Course of CRF

    Staging       GFR         Manifestation     Scr(um

   Compensation     50%~80%       Asymptom      Normal
   Azotemia      25% ~50%     asymptom/symptom    178~ 450
  Renal insufficiency   10%~25%       Asymptom       450~ 70
     Uremia     ﹤ 10%      Uremic symptom     ﹥ 707
GFR Description Treatment stage

1 90+ Normal kidney function but Observation, control of

urine or other abnormalities blood pressure
point to kidney disease
2 60-89 Mildly reduced kidney Blood pressure control,
disease monitoring, find out why.

3 30-59 Moderately reduced More of the above, and

probably diagnosis, if not
already made.
4 15-29 Severely reduced Planning for endstage renal
failure - more info.

5 14 or Very severe See treatment choices for

less endstage renal failure.
Section 2 pathogenesis o f
• 1.mechanism of compensation
(1)reserve capacity of kidney
(2)adaptation of renal function
(3)renal hypertrophy
(4)autoregulation of renal blood flow
2. mechanism of
• (1)intact nephron hypothesis
• (2)trade off hypothesis
• (3)glomerular hyperfiltration hypothesis
• (4)lesion of tubular and interstitial cells
(1)intact nephron hypothesis
(2)trade off hypothesis
(3)glomerular hyperfiltration
(4)lesion of tubular and
interstitial cells
Section 3 Alteration of
metabolism and function
1.alteration of urine
• Polyuria
①flow velocity ↑of original urine
②Osmotic diuresis
③Urinary concentration↓
• Nocturia
• Proteinuria
NPN= BUN + PCr + Uric acid

CCR: creatinine clearance rate

CCR= Ucr × Vu= 90~140ml/min


Ucr: urinary creatinine

Vu : urinary vol per min
Pcr : plasma creatinine
•BUN or PCr is not a early sensitive index to CRF
3.water, electrolytes and acid-
base imbalance
• Na+, H2O,
• K+, Mg2+
• Ca2+ and Phosphorus ?
• Acidosis ?
Hyperphosphatemia and
• P
GFR urinary P
PTH bone salt dissolved
P X Ca2+=40
unsoluble Ca2+ phosphate in gut
gut inhibited by toxin
4.renal hypertension

Renin dependent

Na+ dependent

Renal-deprived vaso-dilating
5.renal osteodystrophy

calcium & phosphate imbalance and PTH ↑

hypocalcemia: 1,25- (OH)2-D3 ↓

6.hemorrhagic tendency
• Plt amount nor, function
7.renal anemia

erythropoietin ↓

bone marrow inhibited

formation ↓
hematopoietic precursor
RBC ↓ damage↑ substance ↓

Section 3 Alteration of
metabolism and function
• 1.alteration of urine
• 2.azotemia
• 3.water, electrolytes and acid-base
• 4.renal hyper tension
• 5.renal osteodystrophy
• 6.hemorrhagic tendancy
• 7.renal anemia
Section 4 prevention and

• See in uremia


Part 4 Uremia
• End stage renal disease

• urine in the blood

• Many toxins
Section 1 pathogenesis o f
• 200 metabolites and toxin uremia toxin
• ( PTH ( guanidine compound )
urea amines )
Uremic toxins
• Protein control in the diet
• Dialysis relief
• Uremic plasma cellular toxicity
(1)retained metabolic products
Asymmetric dimethylarginine
(2)overproduction of counter-regulation
(3)underproduction of renal hormone
Section 2 functional and
metabolic alteration
• (1)nervous system
major manifestation
homeostasis disorder
denaturalization of nerve cell
brain edema
Central neurologic system Lethargy, irritability, frank encephalopathy,
asterixis, and seizures
Peripheral neurologic system
Symmetric sensory neuropathy in a glove-and-stocking distribution
• (2)digestive system
the earliest symptom
observed easily
uretic fetor

• Anorexia, nausea, vomiting and weight loss, which improve

after dialysis is initiated.
• Gastritis, peptic ulceration and arterio-venous malformations
→ gastrointerstinal bleeding
• (3)cardiovascular system
pericardial friction rub
pericardial tamponade
(4)respiratory ~
Kussmaul breath (deep and big
named for Adolph Kussmaul, the 19th
century German doctor who first noted it.
Also called "air hunger."

Cellular immune
T cell
NP chemotaxis
(6)skin changes(dermatologic
• Pallor
• Pruritus and excoriation
• Uretic frost
• Gray discoloration
• Ecchymosis and hematomas
(7) metabolic disorders
• glucose
glucose tolerance
• Protein
Negative nitrogen balance
• Fat
triglyceride hyperlipidemia
Section 3 prevention and
• 1.treat primary disease
• 2.control and prevent aggravating factors
• 3.dialysis
• 4.other treatment
( end )