Renal Intensive 2021

*Cross section & Blood supply:

Filtration occurs across the glomerular basement membrane produced by:

1-The glomerular capillary endothelial cells (contain fenestrae)
2-fusion of the basement membranes of epithelial and endothelial cells
3-glomerular epithelial cells (podocytes) 2
Physiology of urine formation:
1- Glomerular Filtration ( by simple diffusion): 1
contraction of mesingeal cells in afferent & efferent arterioles will lead to increase of
glomerular pressure from 14 mmHg to 60 mmHg so blood filtrate can move from high pressure to low
pressure of bowman's capsule (20-26 mmHg )…… all LMW blood filtrate will move except for proteins
due to negativity of basement membrane.
2- Tubular reabsorption:
Its transport of substances from PCT to efferent arterioles of :
*almost all water *urea * Na * Ca * Glucose * Hco3 * small proteins
3- Tubular secretion:
Its transport of substances from venoues system to DCT : * K *H *Po4
Functions of the kidneys:
1-Filtration of waste products (urine formation)
2-Erythropoietin is produced by interstitial peritubular cells in response to hypoxia.
3-In vitamin D metabolism, (25-hydroxycholecalciferol 1,25-dihydroxycholecalciferol).
4-Renin (RAAS)
5-electrolyte regulation
6- acid base balance (buffering system)

Urine analysis:
1-Colure: normally yellow
DD of Dark urine: MCQ
Schistosoma
1- Hematuria haematobium

2- Hemoglobinuria & Myoglobinuria (No RBC)

Dipstick-negative dark urine
1-Food dyes(beetroot) 2-Drugs:Senna, Rifampicin, Levodopa
3- Porphyria 4- Bilirubinuria
 Causes of polyuria MCQ
2-Urine Volume: (300-2500 ml) 1- Excess fluid intake
Polyuria: >2500 ml 2- hyperglycemia & hypercalcaemia
Oligouria < 400 ml (300) 3- diabetes insipidus
Anuria < 50 ml 4-Drugs/toxins, e.g. lithium, diuretics
3- Glucose : ( no suger ) 5- Interstitial renal disease
Gucosuria : 1- DM 2- Renal failure 6- Hypokalaemia =(Barters syndrome)
3- pregnancy 4- puberty Causes of Oliguria:
MCQ
4- Protein : normaly <140mg/24hurs 1- Urinary obstruction (stones,
Proteinuria: tumors, BPH)
< 500mg/24H : 1- UTI 2- heart failure 2- Lack of renal perfusion(aortic
dissection, shock, HRS)
. 3- multiple myeloma 4- vigorous exercise
3- Rapidly
. 5- Fever 6- Drugs – steroids + NSAIDs + ACEIS
7-Orthostatic protein urea
< 3500mg/24H: Tubuler disease
> 3500mg/24H: Glumerolonephrits ( nephrotic syndrome)

5-Urea level ( < 50 mg/dl) MCQ

High urea:
1-renal failure (70% of kidney function lost so normal level does not exclude renal disease
2- Dehydration 3- UTI 4- high diet proteins 5-GIT hemorrhage
6- multiple trauma 7- burns 8- Drugs – steroids

6- Creatinin level (0.3-1.1) or ( cystatin-c more sensitive): MCQ

high Cr :
1- Renal failure(50% of kidney function lost so normal level does not exclude renal disease)
2- Rahabdomyalisis & crush syndrome
3- Drugs- Trimethoprim & cimetidine & 3rd generation cephalosporin's
Home work: 1001:Q 745

Acute renal failure = (AKI)

Acute renal failure (ARF) it's a sudden and usually reversible loss of renal function,
which develops over days or weeks. Resulting in:
1- retention of waste products ( CP of uremia)
2- electrolytes (1-Na = low 2= Ca = low 3- K= high 4- Pho3 = high)
3- acid base imbalance (PH = uncompensated metabolic acidosis)
Causes:
Pre-renal : ( renal shock) 50-70% 
1- volume depletion --- Hemorrhage , burns ,dehydration, hepato-renal syndrome
2- CVS (CHF + Cardio-renal syndrome)
3- Decrease oncotic pressure : hypoalbuminemia whatever the cause
4- renal artery vasoconstriction  RAS or Drugs (NSAIDs, ACEIs )
Intra – renal 20-30%:
1- ATN 85% --1- ischemia
2-Toxins & pigments ( Hemoglobinurea + Myoglobinurea )
2- Interstial disease 10% =(CTD=SLE, Hemoltic anemia, cancers, Drugs)
3- Glomerular disease 5% Causes of Rahabdomyolysis:
1- extreme physical trauma
Post renal 10-20%: Causes of obstructive uropathy 2-compartment syndrome
3- status epileptics
4- LL ischemia
Clinical picture:
MCQ 5- ethanol
A: CP of uremia 6- snake bite
1-Drowsy + disorientation + headache + Fits & blurring of 7- metabolic disturbance
vision (visual disturbance) + peripheral neuropathy 8- malignant hyperthermia
2- Anorexia , Nausea & vomiting + purities + loss of libido
4- increase risk of infections
5- irritation of small blood vessels & decrease platelet function (Epistaxsis, GIT
hemorrhage )
6- irritation of serous membrane
B- CP due to metabolic acidosis ( Epigastric pain , Kussmal breathing = tachypnea )
C- CP due to electrolyte disturbance ( K= weakness + arrhythmia)
d- CP due to underlining cause ( hypotension , tachycardia, MCQ
Biochemical:
decrease peripheral perfusion except if RAS ) 1-Na = low 2= Ca = low 3- K= high
Investigation: 4- Pho3 = high
5- PH = uncompensated metabolic
CP of Uremia Urea/BUN & Cr = high acidosis
Imaging :
1- ECG to rule out hyperkalemia
Post renal cause YES 2-chest x ray for pulmonary edema
3- investigation to detect cause

Urine analysis NO
Ultra sound
Kidney
Hyderonephrosis
Management
1- Establish and correct Hyperkalemia
2- Correct metabolic acidosis: NaHco3may be used if acidosis is severe PH < 7
3- Establish and correct infections : Gentamycine or Vanco.
4- Establish and correct the underlying cause of the ARF.

Pre renal : Inter renal : Post renal :

1- hypervolemia = IV fluids 1- Treat cause if possible 1- refer to urologist
2- CHF = Dubutamine 2- dialysis
3- edema + diuretics
4- RAS = angioplasty & stent if
stenosis > 70%

Prognosis
In uncomplicated ARF= Good
In ARF associated with serious infection and multiple organ failure, mortality is 50-70%.

Dialysis:

Types: 1- Peritoneal dialysis Advantages:

2- Hemodialysis 1- used in HF
2- does not require anticoagulant
3- no risk of (hypotension, blood porn infection,
Modes of hemodialysis: air embolism)
A-Transit Dialysis Disadvantage:
1- Scribner shunt 2- CV line 1-Infection & peritonitis
2- abdominal structure injury
3- failure
4- hyperglycemia

Indications :
1--Hyperkalaemia > 6.5 mmol/L/ECG changes
2-Fluid overload and pulmonary edema.
3-Metabolic acidosis. PH < 6.
4- Plasma urea > 180 mg/dl & creatinine > 6.8 mg/dL)
5-Uraemic pericarditis/uraemic encephalopathy.
6-Drug toxicity induced AKI
B-Permanent Dialysis= AV fistula
Indications : CRF stage 4 & 5
Home work: 2017: Q1 to Q5
1001: Q 718 – 735– 747 – 752
 Hyperkalaemia Clinic
Its K level > 5.5 mg/dl ( n= 3.5 – 5 mg/dl)
Aetiology :
A- increase endogenous k inside blood:
1-acidosis 2- DKA (DM 1) 3- Drugs :B-blockers, 6-Rahabdomyolysis
4-Massive blood transfusion 5- Excessive K intake( IV fluids + food )
B- Defect in excretion:
1- Renal failure 2- Addison’s disease 3- Drugs :spirinolacton, ACEIs, NSAIDs,
Clinical picture :
1- Patients typically present with progressive muscular weakness MCQ
2- sometimes there are no symptoms until cardiac arrest occurs.
Dx: Typical ECG changes
1-Tented T wave is an early ECG sign,
2-Small P wave 3-Prolonged PR interval
3- widening of the QRS 4- Sine wave
Treatment of severe hyperkalaemia

Protect heart *I.v. calcium gluconate (10 mL of 10% solution)

Shift K into cells 1-Inhaled β2 agonist, e.g. salbutamol
2-I.v. glucose (50 mL of 50% solution) and insulin
MCQ
3-Intravenous sodium bicarbonate
Remove K from body 1-I.v. furosemide and normal saline3
2-Ion-exchange resin (e.g. Resonium) orally or rectally

Home work: 1001: Q614

Chronic kidney disease (chronic renal failure)

Def: an irreversible deterioration in renal function which classically develops over a
period of years--- Initially, it is manifest only as:
1- anemia (due to decrease erythropoietin) 2- a biochemical abnormality.
3- clinical symptoms and signs of uremia + end organ damage
Causes:
1-Congenital and inherited (polycystic kidney disease AD, Alport's syndrome X linked)
2-Diabetis mellitus 20-40% 3-Hypertension 5-20% 4-Interstial disease 20-30%
5- Glomerular disease 10-20% 6-Renal artery stenosis 7- SLE, vasculitis 8-unkown
Classification : According to GFR ( n=> 120 ml/mint)
STAGE GFR CLINICL PICTURE
1 90-120 Asymptomatic
2 60-89 Asymptomatic
3a 45-59 Usually Asymptomatic
3b 30-44 Anemia progressive very slowly
4 15-29 (Electrolyte problems likely as GFR falls)
5 <15 Significant symptom and complications usually present
 1-CRF
Symptom and complications: MCQ 2-DM
CNS & PNS: ( due to Nero synaptic urea deposition) 3-IDA
1- epilepsy 2- flapping tremor 3-glove & stock polyneuropathy
4- Renal encephalopathy ( confusion, disorientation, coma) 5- restless leg syndrome
Skin:
1-prurites (Rx= skin emollients & antihistamine)
2- dark pigmentation (due to melanocyte stimulation by urea )
Respiratory system:
1- kussmal breathing ( due to compensated metabolic acidosis) 2- hiccups
CVS:
1- accelerated HTN due to (Na & water retention + Increase risk of arteriosclerosis)
2- uremic pericarditis
GIT:
1- Anorexia , Nausea & vomiting weight loss 2- uremic fetor
3- Abdominal pain ( due to peritonitis, pancreatitis, peptic ulcer )
Endocrine :
1- decrease insulin clearancehigh insulin which will lead to hypoglycemia
2- menstrual irregularity ( amenorrhea)
3- male = impotance & decrease libido
Bone:
osteoprosis & osteomalacia due to stimulation of osteaclast
Blood:
1-anemia due to (1-decrease erythropoietin production 2- Hemolysis 3-Blood loss
Rx: Doxycyclin
4-Nutritional problems 5-Chronic illness=Normocytic MCC )
2- pancytopenia ( decrease cellular & humeral immunity = high risk of infection )

Investigation: CP of CRF Urea & Cr ----- high 1- Na =low

2- Ca= early low
late high
Small size Ultra sound 3- K= high
4- Po4 =high
Kidney
5-Ph compensated
NO YES MCQ acidosis
6- LDL = High
1- polycystic kidney Urine analysis:
2-RCC 1-glucose urea = DM
3-hydronephrosis 2- hematuria & cast = GN DD of small size kidney:
4- amyloidosis 1-RAS
Management : 2- Chronic pyelonephritis
Stage 1 – 2 – 3 3- Chronic GN
A- Dietary and lifestyle interventions 4- Chronic interstial nephritis
1-preventing excessive consumption of protein 2- decrease salt & K foods
3- Smoking cessation also slows the decline in renal function. 4-Exercise and weight loss
B- Control of blood pressure : aim is 130/80 mmHg for CKD
C- Proteinuria : ACE inhibitors and ARBs are more effective
D- Anaemia: human erythropoietin (S.C) are effective in correcting the anaemia The
target haemoglobin is usually between 10 and 12 g/dL.
E-Acidosis: plasma bicarbonate should be maintained > 22 mmol/L by giving sodium
bicarbonate supplements. If the increased sodium intake induces hypertension or oedema;
calcium carbonate is an alternative.
6-Hyperlipidemia: Omega 3 & statins slow the rate of progression of renal disease
7-Hyperphosphataemia: is controlled by dietary restriction and the use of phosphate-
binding drugs (e.g. calcium carbonate, aluminium hydroxide).
Stage 4 – 5 ( end stage):
* as above + Renal replacement Terapy ( Dialysis OR Renal transplant)
Prognosis :
5 year survival rate=Hemodialysis 90%-Renal Transplant 80%-Peritonial dialysis 50%

Home work: 2017: Q6 to Q9

. 1001: 723 – 729 – 736 – 737 – 740 – 742 – 751
Glomerulonephritis MCQ
Nephrotic syndrome
Def : its syndrome characterized by: 1- Proteinuria 2-Hypoalbuminaemia
3- Generalized Edema 4- Hyperlipidemia
Causes:
A- congenital ( nephrosis AR)
B- Acquired :
1- idiopathic 2- infections ( bacterial, viral, parasite)
3- inflammatory ( RA, PSS, SLE , PAN) 4- Neoplastic (leukemia, lymphoma)
5-Drugs ( D-pencillamine, gold salts , captopril, warfarine, NSAIDs)
6-others ( DM, amyloidosis, sickle cell anemia, Chronic Pyelonephritis )
Clinical picture : MCQ
1- Massive proteinuria > 3.5g/24hurs 2- Hypoalbuminemia
3- Generalized edema (anasarca) 4-hyperlipedimia  xanthelasma + IHD
5-decrease binding globulin of Vit D & Ca
6-decrease AT IIIhypercoagulability DVT , PE, RVT which Predisposes to ARF
7- decrease immunoglobulin's  high risk of infection (peritonitis)
Investigations:
1- 24h/protein 2- serum cholesterol 3-serum protein & albumin
4- Ca level 5-to detect cause& complication 6-Renal US & biopsy (Not always required)
Management:
A-supportive:
1- odema = decrease Na in diet  if not effective give diuretics
2-protein urea = Rx ACEIs 3-infection = Rx Abs + prophylactic vaccine
4- thrombosis = Rx anticoagulants or thrombolytic in RVT
B- Specific according to histological types
 Minimal change focal segmental Membranous nephropathy
nephropathy glomerulosclerosis (FSGS)
Age children(70-80%) Common in adults Commonest in adults
Associated 1-Hodgkins lymphoma 1ry ( idiopatic) Causes:1ry or
disease 2-B.Asthma 2ry alport syndrome 2ry= 1- inflammatory
3-nephritic syndrome vasculitis 2- Neoplastic
sickle cell disease 3-Drugs
heroin & morbid obesity 4- DM & Amyloidosis
CKD NO 1ry = yes 1/3= resolation
2ry = No 1/3= remain nephrotic
1/3 = CKD
Biobsy light microscope= normal multiple renal biobsy Single biopsy
EM =fusion of podocytes
Treatment 1-supportive 1-supportive 1-supportive
2-Steroieds 2-Steroieds 2-Steroieds
3- alkylating agents (e.g.
cyclophosphamide)

Home work: 2017: Q10 to Q14

. 1001: 716 – 720 – 722 – 724 – 728 – 730 – 731 – 738 – 739 – 743 – 746
. – 750 - 753 – 757
Nephretic syndrome

Def : its syndrome characterized by: 1- Hematuria (RBC casts) 2- Oliguria

3- HTN (Na+H2o retention) 4-Proteinuria
Causes:
1- congenital (Alports syndrome)
2- 1ry (idiopatic) Rapied progressive glomerulonephritis
With granular deposition :
1- IgA nephropathy (MCC)
With liner deposition : 2- mesangiocapillary GN
1- Anti glomerular basement 3- Hesscheoline purpura
membrane AB (Goodpasters disease ) (Abdominal pain + lower limb rash)
2ry:- 4- SLE GN
1-Post streptococcal GN (MCC of acute GN)
2- infections viral( Hbv, CMV, EBV ) 3- Neoplastic
4-Drugs (NSAIDs) 5-others (small vessel vasculitis)

Goodpasture's disease (anti-GBM disease)

Usually crescent Linear nephritis along GBM & Alveolar pulmonary membrane due to
Autoantibodies (IgG) (HLA-DR15 + DR2)
Clinical picture: Nephritic syndrome Associated with lung hemorrhage
Dx: chest x-ray white opacity in lower zone Kidney biobsy Cresentric liner
Rx: corticosteroids, cyclophosphamide and plasma exchange
IgA nephropathy (burgers disease) MCQ
most commonly recognized type of GN due to IgA deposition
Clinical picture: Pts has URTIs during or few days later 3days presents with
1-Haematuria is early, proteinuria a later feature, and hypertension common in old.
2-progressive loss of renal function (ESRD.) = 10-20%
Dx: Renal biobsy Mesangial proliferation & IgA deposition +C3 deposition , low
serum complement
Rx: 1-response to immunosuppressive therapy & corticosteroids is usually poor.

Acute post-infectious glomerulonephritis (common in children) MCQ

This is most common post infection with group A –B hemolytic streptococcus (throat
infection=10 days or skin infection=21 day)
CP: An acute nephritis of varying severity occurs:
Nephritic syndrome + hypertension and edema are common
Dx: 1-There are low serum concentrations of C3 and C4
2- evidence of streptococcal infection :(ASO) titre, culture of throat swab
Rx: Renal function begins to improve spontaneously within 10-14 days, and
management by: 1- fluid and sodium restriction 2- diuretic and hypotensive agents.
Prognosis: resolve completely in (90%)

Home work: 2017: Q15 to Q18

1001: Q715 – 721 – 725 – 732 – 734 – 735
* Indications of Renal biopsy:
1- Acute renal failure that is not adequately explained MCQ
2- CKD with normal-sized kidneys
3- Nephrotic syndrome or glomerular proteinuria in adults
4- Nephrotic syndrome in children that has atypical features or is not responding to Rx
5- Isolated haematuria or proteinuria with renal characteristics or associated abnormalities
Renal Artery Stenosis
Significant reduction of renal blood flow occurs when there is more than 70% narrowing of the artery
Causes :
1-Atherosclerotic 2-fibromuscular dysplasia ( In younger female 15–30 years (
3-Rarely, Takayasu’s arteritis and polyarteritis nodosa
Clinical features
1-hypertension 3-progressive renal failure (with bilateral diseas)
2- acute pulmonary oedema 4- deterioration in RFT when ACE inhibitors or ARBs are administered.
Investigations
1-Biochemical testing may reveal:impaired renal function - elevated plasma renin activity-
hypokalaemia due to hyperaldosteronism
2-CT angiography or MR angiography 3-Ultrasound may also reveal a discrepancy in
size between the two kidneys
Management
1-The first-line is medical therapy with antihypertensive drugs,
2-statins and low-dose aspirin
3- angioplasty
Tubulo-Interstitial nephritis
Acute interstitial nephritis (AIN) MCQ
Causes of acute interstitial nephritis
1-Allergic: Many drugs, but particularly Penicillins, NSAIDs , PPIs, Rifampicine
2-Immune: Autoimmune nephritis ± uveitis, Transplant rejection
3- Infections: Acute bacterial pyelonephritis, Leptospirosis , Tuberculosis
4- Toxic: Mushrooms
CP: fever, rash, arthralgia, uveitis + severe ARF
Dx: CBC = High WBC eosinophil's + Urine analysis= leucocyturia (eosinophils70%)
Renal biopsy: polymorphs + lymphocytes + eosinophil's surrounding tubules
Rx: treat cause + High does corticosteroids will accelerate cure for good prognosis
Chronic interstitial nephritis
Causes : 1-Acute interstitial nephritis 2-Glomerulonephritis
CP: Most patients present in adult life with CKD, hypertension and small kidneys
Dx: extensive fibrosis & tubuler loss Rx: as CKD
Renal tubular acidosis (RTA)
To maintain normal PH of urine (4.6 – 8 ) BY 2 mechanisms :
1-reabsorption of bicarbonate in the 2-acid secretion in the distal collecting duct

RTA ('type 1')
due to defect in acid
secretion
causes: 1-Congenital
2-Hyperglobulinaemia
3-Autoimmune connective
tissue diseases, e.g. SLE
4-Toxins and drugs, e.g.
toluene, lithium,
amphotericin
CP: acid accumulation
mobilisation of calcium
from bone osteomalacia
2- hypercalciuria stone
formation and
nephrocalcinosis.
3- Potassium is also lost in
classical distal RTA
Rx: 1- Rx cause 2- NaHco3
Proximal RTA ('type 2')
Due to defect in reabsorption
of HCO3
1-Congenital,e.g. Fanconi's
syndrome, cystinosis, Wilson's
2-Paraproteinaemia
3-Amyloidosis
4-Hyperparathyroidism
5-Heavy metal toxicity
6-Drugs, e.g. carbonic
anhydrase inhibitors
Same
Same
Hyperkalaemic distal RTA (type 4')
due to defect in secretion of both
potassium and acid
1-Obstructive nephropathy
2-Drugs, e.g. amiloride,
spironolactone
3-Renal transplant rejection
same but K is spared
1- diuretics of Fludrocortisones
 Polycystic kidney disease
(PKD) is a common condition that is inherited as an AD.
MCQ
Clinical features
Affected subjects are usually asymptomatic until later life. After the age of 20
common clinical features
1- Vague discomfort in loin or abdomen due to increasing mass of renal tissue
2- Acute loin pain or renal colic due to haemorrhage into a cyst
3-Hypertension
Extra renal CP:
4-Haematuria (with little or no proteinuria) MCQ
1-hepatic cysts 30%
5-Urinary tract or cyst infections 2-Berry aneurysms & SAH 10%
6- Renal failure 3- MR &AR are frequent but rarely severe
Investigations : 4- colonic diverticulae and hernias
1- family history & clinical findings. N.B: PKD is not a pre-malignant condition.
2-Ultrasound demonstrates cysts in approximately 95%
Rx:
1- Good control of blood pressure is important 2- dialysis and transplantation.
3- Rx complication
Home work: 2017: Q19 to Q21
. 1001: Q719 – 727 – 741