2. Very old pic. of KAABA

3. BY DR WAQAR MBBS, MRCP ASST. PROFESSOR
RENAL FAILURE BY
DR WAQAR
MBBS, MRCP
ASST. PROFESSOR

4. NORMAL FUNCTIONS OF THE KIDNEYS
Excretion of wastes ( Urea, creatinine )
Acid-base balance ( excretion of acids produced in the body)
Electrolyte balance ( Na, K, P etc)
Erythropoeitin production ( for RBC synthesis). It is a hormone.
Salt & water balance maintain BP
Activate Vit D, thus managing Ca & Phosph.

5. EFFECTS OF RENAL FAILURE
High urea & creat. ( uremia)
Acidosis
High K & P, low Na
Decreased erythropoeitin anemia
Poor water excretion HTN,CHF
No Vit D activation Vit D deficiency
* Low Calcium * High phosph. * high
parathyroid
hormone

6. TYPES OF RENAL FAILURE ACUTE ( ARF) CHRONIC (CRF)
ARF : Sudden loss of renal function which develops over few days to wks. Creatinine rises & GFR falls in a short time.
CRF : Persistent renal failure for more than 3 months. It is progressive & longstanding

7. REMEMBER
The level of creatinine does not tell you whether the renal failure is acute or chronic. It just tells you the severity of the disease
Eg:
A patient with ARF can have creatinine: 5
A patient with CRF can have creatinine: 3

8. S/S of Renal Failure
Gen.: * weakness, fatigue, nausea & vomiting ( very common presentation)
Features of anemia
Nervous system: : Uremic encephalopathy (siezures, coma, mental changes etc) or peripheral neuropathy
CVS : * Pericarditis * Pulm edema( if fluid
overload ) * HTN
Platelet dysfunction: * Bruising * epistaxis
Skin : * Itching ( due to high Phosphorus)
Bone : * Bone pain & fractures ( Vit D defi.)

9. ELECTROLYTE DISTURBANCE IN RENAL FAILURE
High K
High Mg
High P
Low : Calcium

10. TYPES OF ARF (AKI) ( Based on the site of the problem)
Pre-renal : Decreased renal blood flow
Renal : Diseases in the kidney
Post-renal : Obstruction “beyond” the kidney
Combination of the above can also occur

11. PRE-RENAL ARF
ETIOLOGY : Decreased blood supply to kidneys * Hypovolemia ( blood loss, severe dehydration) * Hypotension * CHF ( decreased effective circulating vol.) * Renal artery stenosis (bilateral) * Liver cirrhosis ( decreased blood flow to the kidneys)

12. WHEN TO SUSPECT PRE-RENAL ARF
1) See the whole situation ( bl. Loss, dehydration) 2) Suspect pre-renal failure in hypovolemic patients. The following indicate hypovolemia: * Low BP, High pulse * Orthostatic changes ( when a supine pt. sits or stands, systolic BP falls more than 20, & pulse rises more than 10. This is abnormal)

13. INVESTIGATIONS IN PRE-RENAL ARF
BLOOD: * High urea & creatinine * K+ & P URINE: * Decreased amount (oliguria) * Osmolality & sp.gravity are high ( urine is concentrated ( Just imagine that the kidney is conserving water)

14. PRE-RENAL ARF TREATMENT
I.V. fluids, blood ( according to the situation)
Treat the cause ( CHF etc)
With correct Rx, renal perfusion improves & so
urine output improves.
If it is not treated soon, renal hypoperfusion can
damage the tubules

15. POST-RENAL ARF
This occurs due to obstruction of the urine flow, anywhere beyond the kidney
Obstruction should be bilateral.
Etiology :
* BPH ( benign prostate hypertrophy)
* Urethral stricture * Cancer of bladder
* Large stones in both ureters

16. ON EXAM:. Enlarged prostate ( if BPH)
ON EXAM: * Enlarged prostate ( if BPH) * Palpable bladder ( Not palpable if obstruction is in the ureters) * Palpable kidneys (hydronephrosis)

17. INVESTIGATIONS IN POST RENAL ARF
1) Ultrasound : Shows BPH, hydronephrosis, hydroureter, stone etc ( depending on pathology) 2) Other routine tests ( high crea., high K) 3) Intravenous pyelogram. A contrast is injected & then Xray pictures of the kidney are taken Any patient with Renal failure should be examined & investigated for obstruction

18. Ivp (intra venous pyelogram)

20. TREATMENT DEPENDS ON THE SITE OF OBSTRUCTION In BPH:
* Drain the bladder w/ Foley’s cath ( acute
treatment)
* Rx of BPH ( medicines or surgery)
2) In Ureteric obstruction (eg stones)
* Drain the ureters by stent
* Definitive treatment of obstruction (surgery,
lithotripsy in case of stones)

21. In acute renal failure due to obstruction,once the obstruction is removed, there is post obstructive diuresis which can cause fluid & electrolyte loss. So, check and manage fluid and electrolytes ( very important)

22. Stent

23. INTRINSIC RENAL ARF
Renal failure is due to disease in the kidneys Tubular Glomerular Interstitial damage damage damage Commonest cause is tubular damage

24. Things which can damage the tubules
Prolonged ischemia ( decreased blood flow)
i.v.contrast
Drugs (medicines)
Uric acid
Pigments ( eg hemoglobin)

25. Causes of Tubular damage ( acute tubular necrosis ATN)
Ischemia to the tubules:
*Due to prolonged ischemia(hypovol, hypoten.)
* Damaged tubules can’t absorb water & Na
* So too much water & electrolyte loss
* Recovery in 1 to 3 wks ( 85% cases) if the kidneys were normal before.

26. Other causes of Tubular Damage
2) i.v. contrast : Can damage tubules * More chances in DM, CRF, dehydrated pt. * i.v. fluids before X-ray procedure reduces the risk 3) Drugs : Aminoglycosides, NSAIDs 4) Pigment nephropathy: * Hb.: In hemolysis. * Myoglobin : In muscle injury ,eg. car accidents, vigorous exercise.

27. 5) Tubule damage by uric acid
5) Tubule damage by uric acid * Happens in cancers when chemotherapy is started & there is too much breakdown of cells, which releases uric acid. * This is called TUMOR LYSIS SYNDROME. It can cause acute renal failure due to tubule damage by uric acid Tubular damage due to any of the above, produces “granular casts” in the urine ( what are casts, remember?)

28. GLOMERULAR CAUSES OF ARF
Various glomerulonephritis can cause ARF
Urine shows : “Deformed” RBCs, RBC casts,
& proteinuria
INTERSTITIAL DAMAGE CAUSING ARF
Also called “interstitial nephritis”
Commonest cause : Antibiotics ( PCN, Cephalosporins), Infections, NSAIDs
Urine : * WBC casts * eosinophils

29. URINALYSIS HELPS A LOT IN ARF
Pre-renal ARF
Renal-ARF
Urine osmolality >500 mosm. ( high)
( Urine is very concentrated)
* < 350 ( low) ( Tubules are damaged and lost their concentrating ability. So urine is very dilute)

30. Other Urinalysis Features
Granular Casts : suggest ATN (tubular damage)
RBC casts : suggest glomerular lesion
WBC casts : suggest interstitial nephritis
Crystals : seen in uric acid nephropathy
( uric acid crystals)

31. TREATMENT OF ARF
Treatment is mostly supportive ! 1) Manage vol. status: * If hypovol., give fluids * If fluid overload, give diuretics * Strict Intake /output charting, daily wt. 2) Correct Electrolyte problems: eg hyperkalemia & hypermagnesemia . Check daily 3) Manage acidosis: Na. bicarbonate 4) Assess the pt. daily to see if he needs Dialysis 5) Adjust the doses of any drugs given( v. imp)

32. PROGNOSIS OF ARF Depends on the cause
Commonest cause of death is sepsis (impaired immunity due to uremia)
In some patients, renal function recovers in 3-4 wks
In others, renal damage becomes irreversible
leads to CRF (chronic renal failure)

33. CHRONIC KIDNEY DISEASE
DEFINITION : Impairment of kidney function which persists for > 3 months. It is usually progressive
ETIOLOGY:
DM MOST COMMON CAUSES
HTN
Any chronic disease of renal parenchyma
( the causes of ARF can become chronic also)

34. Etiology contd.
4) Polycystic disease (ADPKD) 5) Chronic “B/L” obstruction * Prostate hypertrophy

35. STAGES OF CKD (CRF)
Renal failure is divided into 5 stages, based on the GFR (glomerular filtration rate). Normal GFR > 90ml/min ( it means that in 1 min., > 90 cc of fluid is filtered at the glomerulus). As renal failure progresses, GFR falls.

36. STAGES OF CKD
Stage GFR 1 >90 cc 2 b/w b/w b/w less than 15 Initial stages may be asymptomatic. S/S & complications usually develop from Stage 3 & down

37. TREATMENT OF CRF
In the treatment of CRF, we basically manage the complications which have happened. First we try conservative/medical treatment. If that fails, then dialysis or renal transplant.

38. TREATMENT OF CRF DIET RESTRICTIONS:
Low protein diet ( coz urea/creat. are formed from
protein)
( excess proteins damage the kidneys more)
b) Restrict K ( it is high in renal failure)
* Stop bananas, tomato, potato
* May need drugs which bind with K in the GIT to
prevent its absorption ( K binding resins)
c) Restrict dietary “P” * Dairy products, * nuts
( MUKASSARAAT) * May need phosphate binders
eg CaCO3 tablets
d) Salt & water restriction if there is HTN &
pulmonary edema

39. Rx. (contd).
2) HTN : * Tight control v. imp * Aim: < 130/80 * Best are ACE inhibitors ( follow K & crea) 3) Anemia: Cause is erythropoeitin deficiency & also Fe deficiency (due to GI bleeding) * Check for Fe def. first, & treat if present * Then give erythropoeitin Injecs. (Given long term) ( don’t raise the Hb. more than 12)

40. S/E of ERYTHROPOEITIN * HTN * SIEZURES

41. 4) BONE DISEASE IN CKD (renal osteodystrophy) No activation of Vit D in CKD so lack of vit D so low serum Ca & high P this causes release of PTH( sec. hyperparathyroidism) bones become weak (osteomalcia,osteoporosis) * Rx : Give Calcium & Vit D tablets ( long term). This will correct the Ca, P & also PTH levels

42. CRF COMPLICATIONS contd.
5) ACIDOSIS : Due to accumulation of acids. * Give Na bicarbonate tabs 6) Pneumovac & flu vaccine 7) Neuro. S/S : * Neuropathy ( all types : sens, motor, auton.) * Confusion,dementia,siezures TREATMENT OF NEURO S/S IS DIALYSIS. 8) PERICARDITIS: Rx is dialysis

43. Dont forget to adjust the doses of medicines in patients with renal failure.