This ppt explains and simplifies CKD for medical students

1. CHRONIC KIDNEY DISEASE(CKD)
LUKAS SALUNDA
5TH YEAR -CBU(SOM).

2. CHRONIC KIDNEY DISEASE
 This is the progressive and irreversible damage of the nephrons and glomeruli.
 It is CKD when it is greater than or equal to 3 months.
 In most cases the signs begins to show when GFR is less than or equal 90.

3. CAUSES
 The leading causes are diabetes and hypertension.
 Some other causes are;
1.Renal Artery stenosis
2. Polycystic kidney disease
3. Tubulointerstitial disease
4. Lupus
5. Amyloidosis
6. Repeated episodes of pyenephritis
7. Prostate cancer e.t.c

4. HYPERTENSION
 Long standing HTN, thicken vesssels in kidneys to withstand the pressure.
 Done by high protein deposit on these vessels and in turn lead to hyaline artery
stenosis.
 Materials such as oxygen are affected and cause less delivery.
 E.g mesangial cells which acts as the supporter of the glomerus, are starved of
oxygen.
 reduced oxygen Ischemia Necrosis Activates mesangial cells.
 Activated mesangial cells secretes transforming growth facror beta.

5.  The TGF-Beta then leads to fibrosis of the glomeruli sclerosis.
 The area of g;omerus becomes even more harder, thicker and bigger.
 As a result, it reduces the glomerular filtration rate and it is stays more than or equal
to 3 months, that is now CKD.
DIABETES
When there is too much glucose in the blood of kidney vessels, it can combine with
proteins and lipids in the process called non-enzymatic glycation and produces some
proinflammatory molecules.
And this later causes damage such as arteriosclerosis and atherosclerosis plaques to
the vessels.

6.  Affects efferent vessels, later lead to backflow pressure and cause raised GFR.
 Raised GFR activate mesangial cells and they will secrete TGF-Beta, leads to fibrosis
and causes glomeruli sclerosis and this will reduce GFR.
 The efferent Artery also supply blood to the tubular vessels but if affected, there will
be less oxygen being delivered which leads to tubular diseases and this will mean
reduced GFR.
GLOMERULONEPHRITIS
In some people with ilnesses such as HIV/AIDS and Hepatitis, their immunity reacts
and produces the abnormal antigen-antibody complex which is mostly deposited at the
glomerulars basement membrane.

7.  It activates inflammatory processes and damage the glomerula basement membrane.
 And this makes it to allows large substances to pass through which should not initial
do.
 But mesangial cells try to avoid that and so they secrete TGF-Beta which leads to
fibrosis and later arteriosclerosis and finally reduced GFR.
POLYCYSTIC KIDNEY DISEASE
These begin to compress vessels and reduces blood flow and oxygen and leads to
ischaemia which causes necrosis and finally reduction in GFR.
Juxtaglomerular cells will secret renin.

8.  Leads to the raise in BP in the vessels by vasoconstriction caused by the action of
angiotensin II
 The raised BP leads to glomerulosclerosis and may drop the GFR and the raised BP
is the secondary type of HTN.
NSAIDS
PGI2 and PGE2 causes vasodilation in Afferent arteries and so more blood to the
glomerular and high GFR.
NSAIDS block them and leads to vasocontriction and later reduced GFR and if it
persists for so long then it is CKD.

9. PATHOPHYSIOLOGY
1. ELECTROLYTE IMBALANCE
 Normally potassium and phospate should be excreted by the kidneys.
 But reduced GFR, there will be less filtration of these elements and this
will make them accumulate in the blood.
 Even the enzyme alpha-1 hydroxylase will decrease and this reduces
Vitamin D.
 Reduced Vitamin D, will affect the reabsorption of calcium and cause
hypocalcaemia.

10. 2. WATER IMBALANCE
 Reduced GFR leads to less water filtered and so more water retension and go into
tissue of organs;
1. lungs Pulmonary edema
2. Heart HTN
3. Legs Peripheral edema
Due to kidney damage, albumin also lost and it keeps water in the vessels, so there is
loss of water into the interstitial space and leads to fluid overload.

11. UREA
 Azotemia; urea build up but not affecting tissues or organs
 Uremia; urea causing damage to the tissues and organs e.g encephalopathy,
seizures, coma, fatigue, nausea and vomiting.
 Can irritate the pericardial and lead to inflammation and fluids in the pericardial
space, this is called uremic pericarditis and can sometimes cause pericardial
effusion.
 Sometimes sips into the sweat glands and they bring them out on the skin and
cause uremic frosts.

12.  Also stick to the platelets and makes them not to aggregate to each other and in turn
cause bleeding.
HORMONAL IMBALANCE
Kidneys secretes erythropoietin which stimutes the red bone marrows to undergo
erythropoiesis.
So reduced erythropoietin lead to the type of anaemia called anema of the chronic
disease.
Liver adds a group of 25 hydroxycholecalciferol to the inactive vitamin D and alpha -
1 hydroxylase from the kidney does the work to form 1,25 dihydroxycholecalciferol the
most active form of vitamin D.

13.  Decreased process, there will be low Vitamin D and so low calcium absorption.
 So parathyroid is triggered to secrete parathyroid hormones and since they can not
reabsorb it from the kidneys, they make osteoclast to undergo bone resorption.
 But bones being the only source, more bones are destroyed and calcium level raised.
 Lead to alot of diseases such as renal osteodystrophy, osteitis fibrosa cystica and also
fracture.
ACID-BASE IMBALANCE
The alpha intercalated cells on the cortical collecting duct which secretes hydrogen
and absorb Bicarbonate.
Decresed excretory of hydron ions makes it accumulate in the blood and cause
metaboilc acidosis.

14.  So more Bicarbonate lost in urine and reduces in the blood contributing to acidosis,
bicarbonate lost in urine.
ALBUMIN DISORDERS
When the glomerular basement membrane damaged, it spills albumin and lost in the
urine
So promotes protein synthesis but lipoproteins increases more. Hence, Triglyceride
and low density lipoproteins are raised and end up in hyperlipidermia state.

15. CLINICAL FEATURES
 Nausea
 Vomiting
 Loss of appetite
 Fatigue and weakness
 Sleep problems
 Urinating more or less
 Decreased mental sharpness
 Muscle cramps

16.  Swelling of feet and ankles
 Dry, itchy skin
 High blood pressure (hypertension) that's difficult to control
 Shortness of breath, if fluid builds up in the lungs
 Chest pain, if fluid builds up around the lining of the heart

17. CLASSIFICATION OF CKD
 Can be classified according to;
1. GFR
2. ALBUMINURIA
3. RIFLE
4.KDGO
They can help us know the type of treatment to take.

18. 1. ACCORDING
TO GFR.
As GFR decreases, the
level of the disease
increases .

19. 2.
ALBUMINURIA
Also called the
predictor of the
disease.
The more albumin,
the severe is the
disease.
We use Urine
Albumin to creatinine
ratio.

20. 3. RIFLE

22. DIAGNOSIS
 Combination of Clinical features and Investigations
INVESTIGATIONS
1. GFR
Determined by using creatinine.
Normal average value(125ml/min).

23. 2. ALBUMINURIA
3. RENAL ULTRASOUND
Helps detect the cause of CKD, can detect Polycystic Kidney Disease.
Also look at vascularity and in case of decreased vascularity.
4. RENAL BIOPSY AND SEROLOGY
Biopy do a lot of studies and help detect the cause,
Seriology, helps in the case of immune mediated cause, we can do ANA, RF, HIV and
hepatitis.

24. ADDITIONAL LABS
1. BASIC METABOLIC PANEL(BMP).
Checking potassium, phosphate, calcium and sodium mostly.
2.FBC
Checking for anaemia( Normacystic type).
We can add iron study.
3.ABG
Mostly show acidosis

25. 4. LIPID PANEL
 Check for Triglycerides and low density lipoproteins.
We can also check PTH to check phosphate levels in case of severe CKD.
There also other tests done depending on the presentation of the disease and the
clinician.

26. TREATMENT
 Principles are to;
1. preserve the remaining renal functions.
2.Avoid further Injury( progression).
3. Corrections of the imbalances.
4. Treating the cause.

27. HYPERTENSION
 Treat it and the goal is to reach BP of 130/80mmHg.
 Give ACE-I, ARB’s, k+ sparing diuretic ( block aldosterone) and other
diuretic to remove water (overload).
DIABETES
Life style modification e.g diet.
The goal is to reach HBAc of atleast 6.5%
Give insulin in type I and Anti-diabetic type II.

28. 3. GLOMERONEPHRITIS
 Treat underlying cause of GN
 Give steroids after seeing the cause, also demads are used.
4.PCKD
Treat secondary HTN.
If too bad, renal transplant.
5. NSAIDS
Discontinue
Also other nephrotoxic Drugs.

29.  The rest you treat according to finding e.g treating anaemia, giving calcium or
vitamin D, replace hormones such as EPO e.t.c.
 For TG and LDL, give statins and desmopressin (DDAVP).
 But if CKD worsen and there are AEIOU, reduced GFR and other complications it is
to use dialysis as a bridge to transplant.
COMPLICATIONS
Fluid retention, which could lead to swelling in your arms and legs, high blood
pressure, or fluid in your lungs (pulmonary edema)
A sudden rise in potassium levels in your blood (hyperkalemia), which could impair
your heart's function and can be life-threatening

30. Anemia
Heart diseases
Weak bones and an increased risk of bone fractures
Decreased sex drive, erectile dysfunction or reduced fertility
Damage to your central nervous system, which can cause difficulty concentrating,
personality changes or seizures
Decreased immune response, which makes you more vulnerable to infection
Pericarditis, an inflammation of the saclike membrane that envelops your heart
(pericardium)
Pregnancy complications that carry risks for the mother and the developing fetus
Irreversible damage to your kidneys (end-stage kidney disease), eventually requiring
either dialysis or a kidney transplant for survival

31. QUESTIONS
NATOTELA.