Nephro Key Flashcards
1
Q
Rhabdomyolysis
• As skeletal muscles are dying → they release (Myoglobulin, Potassium,
Creatine Kinase…).
• Common Scenarios and Hints: (Important √)
A
√ A person was trapped for several hours under a heavy object.
√ A fall followed by a long period of lying on the floor.
√ An elderly with frequent falls presents with Acute kidney injury.
√ IV drug abuser was found on the floor not moving for a long period.
√ Long-distance run (eg, Marathon runner) “Severe Exertion/ Severe
Dehydration”.
√ Severe Crush injury.
√ Exercise-induced rhabdomyolysis (e.g. in athletes)
2
Q
A
3
Q
• Myoglobulin is nephrotoxic and thus can lead to Acute Kidney Injury (AKI).
Therefore, rehydration with is an essential initial step.
That’s why
Rhabdomyolysis is a medical emergency that you have to be aware of!
IV fluid •
ECG must be performed as the released potassium from the dying muscles
(hyperkalemia) can be dangerous.
If ECG changes suggesting hyperkalemia
(Tall tented T wave, Wide QRS) are found:
→ Protect the heart by giving I’ve calcium Chloride or calcium gluconate before anything else!
A
± Hematuria (Reddish Brown or Tea-coloured urine) (False Positive as the
cause of redness is myoglobulin (which has heme), while RBCs are not found in
urine dipstick).
± Hypotension.
± AKI “Acute kidney injury” → (High urea and Creatinine).
± Very high CK (Creatine Kinase).
√ Although uncommon, one of the side effects of statins is Rhabdomyolysis. √
4
Q
◙ Important points on Rhabdomyolysis:
A
√ Main Complications of Rhabdomyolysis → AKI and Hyperkalemia.
√ Initial management → (to try to avoid acute kidney injury).
√ Initial Investigation for management → ECG
√ If Tall T wave, Wide QRS, the initial line → (Creatine Phosphokinase) “it indicates muscle
give IV calcium chloride/ gluconate.
CPK level √ The best initial test that is specific for Rhabdomyolysis → Urine analysis →
Reddish-brown (Tea-coloured) → Falsely +ve hematuria.
√ To confirm → necrosis”.
√ Other lines of treatment include: Sodium Bicarbonate
▐ Dialysis (in severe cases)
5
Q
Elaboration
Example (1),
A man has just finished a long-distance run and presents with myalgia, red-
brown urine.
Urine dipstick is positive for blood but without RBCs on
microscopy.
ECG shows Tall T waves, Widened QRS and small P waves.
• The initial step in management
A
It is obvious he has Rhabdomyolysis.
As there are ECG changes suggesting Hyperkalemia,
we should protect the
heart before anything else by giving IV Calcium. First things First!
Otherwise, IV fluid is the initial step.
6
Q
IV fluid normal saline.
Myoglobin “reno-toxic”
Example (2),
24 YO mountain climber was rescued after being trapped under a heavy rock
for about 10 hours.
He has dark urine with impaired creatinine and urea.
His
SBP is 100 mmHg and HR is 125 bpm.
A
• The most appropriate management →
• The likely cause of his renal failure →
Myoglobin is renal toxic
√ He has Rhabdomyolysis (Skeletal muscle breakdown due to crush injury or
prolonged immobilised muscles).
√ As the question did not mention ECG changes of hyperkalemia (e.g. Tall T
wave),
the initial step would be IV fluid rehydration to try to avoid further
renal damage.
√ Myoglobin is Nephrotoxic
7
Q
Example (3),
A 22 YO Known HIV Positive male was found comatose on the floor by his
friend. He was not seen for 2 days. On the ED, the patient is confused and
disoriented.
His labs reveal serum Urea level of 47 mmol (normal: 2-7) and
Creatinine 1070 (Normal: 70-150). Sodium is normal, Potassium is 5.6.
The best investigation to perform
A
→ √ This is most likely a case of Rhabdomyolysis.
Creatine Kinase.
√ Prolonged immobilisation (e.g. in coma)
→ Muscle Ischemia → Release of
myoglobin, Creatine Kinase, Potassium and others → Acute Kidney Injury (as
seen here).
√ To confirm → Serum CPK “Creatine PhosphoKinase”.
√ Note, if the Potassium is ↑ and the “ECG” is given as an option, pick it
especially if the question asks about the “initial” step.
8
Q
Example (4),
A 60 YO man known case of hypertension, diabetes mellitus and a previous TIA
presents complaining of a 5 day of diffuse muscle pain and weakness in his
lower limbs.
He is on: ramipril, bisoprolol, aspirin, metformin and simvastatin.
His urine shows myoglobin.
His kidney function tests are deteriorated. His
serum creatinine kinase (CK) is 3000 (Normal: 45-260).
A
√ The likely Dx → Rhabdomyolysis.
√ The likely causing medication that needs to be stopped → simvastatin
Although uncommon, one of the side effects of statins is Rhabdomyolysis.
9
Q
Example (5),
A man had a wardrobe over him for a long unknow period. He was taken to the
ER. He is confused and disoriented. What is the most appropriate
investigation?
A
→ Creatine Kinase.
10
Q
A
11
Q
Acute rapidly progressive glomerulonephritis [+] Pulmonary alveolar hemorrhage
Expressed as:
Hematuria (Kidney involvement) [+] Hemoptysis (Lung involvement)
[+] Impaired KFTs, obviously.
◙ The most appropriate “initial” investigation
→ Anti-glomerular basement membrane antibodies (Anti-GBM antibodies)
◙ The most “accurate” investigation
A
Goodpasture Syndrome
Most accurate investigation
→ Lung or Kidney Biopsy “Crescentic Glomerulonephritis”
• Chest X-ray → Patchy interstitial infiltration (Intra-pulmonary bleeding)
12
Q
Goodpasture
Syndrome (GPS)
A
Hemoptysis + Hematuria
(Lung + Kidney only)
(Abnormal Urea and Creatinine)
Anti-Glomerular
Basement Membrane
Antibodie.
13
Q
GPS (Hemoptysis + Hematuria)
+ Cannot see
(X-linked)
+
Cannot hear
A
Alports syndrome
14
Q
Hemoptysis + Jaundice (Liver)
A
Alpha-Antitrypsin
deficiency
15
Q
Asthma, Eosinophilia
Other organs
p-ANCA
(Eosinophilic
+
Granulomatosis
with Polyangiitis)
A
Churg strauss
16
Q
Wegener’s
Granulomatosis
(Granulomatosis
with Polyangiitis)
A
Upper Respiratory problems
c-ANCA
(Sinusitis/ Nasal septum
perforation/ Epistaxis)
+ Hematuria.
17
Q
Hemolytic-ureamic
Syndrome (HUS
A
Diarrhea that turns to bloody
Syndrome (HUS)
diarrhea + Hematuria (AKI)
18
Q
The sentence “itching after a hot shower” does not always mean Polycythemia
rubra vera (PRV)!
◙ Itching (worse after hot bath) + Pale skin + Peripheral Oedema + ↑ Skin
Pigmentation + (lethargy, tiredness
A
→ Chronic Renal Failure
√ Itching ► due to ↑ serum urea “Uremia” (seen in late stage renal failure).
√ Pale, Tiredness ► due to ↓ Erythropoietin and thus Anemia.
19
Q
Itching in ckd
A
→ Chronic Renal Failure
√ Itching ► due to ↑ serum urea “Uremia” (seen in late stage renal failure).
√ Pale, Tiredness ► due to ↓ Erythropoietin and thus Anemia.
20
Q
Ckd vs liver failure
A
Peripheral edema and hyperpigmentation are also seen in CKD.
√ Note that in liver failure → Ascites, Jaundice, bleeding.
21
Q
Polycythemia rubrA Vera
Ckd
Vs scabies
Itching dd
A
◙ Itching (worse after hot bath) ± Red skin “Flushed/ Plethora due to ↑ Hb” ±
Splenomegaly ± Burning sensation in fingers and toes ± Gout + High Hb
→ Polycythemia Rubra Vera.
◙ Itching (worse after hot bath) + Linear tracks on skin (Burrows)
→ Scabies.
♦ PRV → Red ▐ ♦ Liver Failure → Yellow “Jaundice” ▐ ♦ CRF → Pale
22
Q
◙ Hyponatremia after inadequate IV fluid treatment could be dilutional
◙ Hyponatremia can occur after inappropriate IV fluid therapy such as by
using 5% dextrose. This is called (Iatrogenic cause)
A
.
◙ In sepsis, the allowed IV fluid is either Ringer Lactate or NS (0.5% NaCl), these
won’t cause dilutional hyponatremia.
◙ Hyponatremia after inadequate IV fluid treatment could be dilutional.
23
Q
Example,
A patient with abdominal sepsis (e.g. biliary sepsis) was treated with IV
antibiotics and IV fluids.
Later on, he was found to be hyponatremic (127
mmol/L) with normal Potassium and Normal kidney function tests (Urea and
Creatinine).
A
The likely cause → Iatrogenic.
Normal Serum Na+ → 135-145 mmol/L
24
Q
√ “The kidneys need to remain well hydrated/ perfused to avoid acute
“tubular” necrosis”.
√ “Prolonged ischemia → “low perfusion” to kidneys → Dying tubules =
necrosis = Acute tubular necrosis → AKI”
A
◙ Massive hemorrhage (e.g., during surgery) and hypotensive shock + High
(ATN) (high creatinine)
the commonest renal cause of
acute kidney injury Is acute tubular necrosis.
25
Allergy (e.g., drug intake followed by rash, fever)
+ Hematuria +
↑ creatinine.
Acute Interstitial Nephritis example:
26
→ 1,25-dihydroxyvitamin D.
Formation
√ 25-alpha-hydroxylation of vit. D occurs in → Liver.
√ 1-alpha-hydroxylation of vit. D occurs in → Kidney.
25-hydroxyvitamin D is formed in liver → Then, an enzyme called (1-alpha-
hydroxylase) in kidneys converts it to the active form, which is
→ 1,25-dihydroxyvitamin D.
27
So, why is there vitamin D deficiency in chronic renal failure?
→ due to reduced activity of 1-alpha-hydroxylation.
So, why is there vitamin D deficiency in chronic renal failure?
→ due to reduced activity of 1-alpha-hydroxylation.
Mnemonic
(K) before (L) in alphabetics.
(1) before (25)
Kidney → 1 ▐ Liver → (25)
Another mnemonic
1K
1=Kid
28
29
Chronic and Acute Pyelonephritis
When you see Hypertension + Hx of repeated urinary tract infections (UTIs)
→ Think of:
CHRONIC Pyelonephritis
Repeated UTIs → Renal Scarring →
Chronic Pyelonephritis → Hypertension
30
When you see LOIN/BACK pain + Features of UTI → Acute Pyelonephritis.
Do not get fooled by the patient being pregnant.
Remember ,preeclampsia , occurs after the 20th week of gestation + Hypertension + Proteinuria.
31
Quick Important Notes (Contrast-Induced Nephropathy).
• To reduce the risk of contrast-induced nephropathy in patients with chronic
kidney disease,
adequate hydration is crucial.
• Administering 0.9% normal saline intravenously before and after the contrast
exposure is the most effective method.
• This approach helps to maintain renal perfusion and dilute the contrast
agent, reducing its harmful effects on the kidneys.
32
Scenario Example:
A 65-year-old woman presents to the Emergency Department with severe
fatigue and shortness of breath. She has a history of hypertension and chronic
kidney disease.
On examination, her heart rate is irregular, and she is
noticeably confused. An ECG shows tall, peaked T-waves. Blood tests reveal the
following results:
• Sodium: 132 mmol/L (135-145)
• Potassium: 7.1 mmol/L (3.5-5)
• Urea: 25 mmol/L (2.0-7)
• Creatinine: 480 µmol/L (70-150)
• eGFR: 18 mL/min (>90)
The decision is made to commence emergency hemodialysis. Which of the
following is the most appropriate reason for initiating hemodialysis in this
patient?
A) High serum creatinine.
B) Hyperkalemia.
C) Low eGFR.
D) Hyponatremia.
E) Toxin removal.
Hyperkalemia Answer → B) is the primary indication for initiating emergency
hemodialysis in this scenario due to the immediate risk posed by high
potassium levels and the associated ECG changes.
Immediate treatment may include intravenous calcium to stabilize the cardiac
membrane
and insulin plus dextrose to drive potassium back into cells.
Why Not the Other Options?
1. High Serum Creatinine:
o Elevated creatinine indicates poor kidney function but is not an emergency
indication for hemodialysis unless accompanied by severe symptoms or
complications like hyperkalemia.
2. Low eGFR:
o Indicates reduced kidney function. While it is an important marker, it alone
does not necessitate emergency hemodialysis without life-threatening
complications.
3. Hyponatremia:
o Mildly low sodium levels are not typically an emergency indication for
hemodialysis. Hyponatremia is usually managed with other treatments
unless it is severe and symptomatic.
4. Toxin Removal:
o This is relevant if there is a known toxin or drug that needs to be cleared
from the body. In this case, no such toxin is mentioned, so it is not the
primary reason for dialysis.
Correct Option: Hyperkalemia:
• Reason: Hyperkalemia is a life-threatening condition that requires
immediate intervention due to the risk of cardiac arrhythmias, as indicated
by the tall, peaked T-waves on the ECG.
33
Haemodialysis in Emergency Settings
Introduction:
Hemodialysis is a critical intervention in emergency settings to
correct
life-threatening complications arising from renal failure.
It involves the
removal of waste products and excess substances from the blood
when the
kidneys can no longer perform these functions adequately.
Indications for Emergency Hemodialysis:
1. Hyperkalemia:
o Particularly urgent when serum potassium levels exceed 6.5 mmol/L or
even lower levels if accompanied by ECG changes such as tall, peaked T-
waves.
o Immediate treatment may include intravenous calcium to stabilize the
cardiac membrane and insulin plus dextrose to drive potassium back into
cells.
2. Acute Pulmonary Edema:
o Occurs due to fluid overload that is unresponsive to conventional medical
treatments such as diuretics.
3. Metabolic Acidosis:
o Severe acidosis (pH < 7.1) that does not respond to standard medical
management, requiring immediate correction.
4. Uremic Complications:
o Including conditions such as pericarditis, which result from the
accumulation of uremic toxins in the body
34
Procedure and Preparation: of hemodialysis
• Vascular Access:
o Temporary access via a central venous catheter is typically required to
initiate hemodialysis swiftly in an emergency setting.
• Time and Coordination:
o The process involves coordination with a renal team, preparation of the
dialysis machine, and ensuring adequate vascular access,
which can take
from 30 minutes to several hours depending on the patient's condition and
available resources.
35
Scenario
A 55-year-old woman presents to the clinic for a routine follow-up visit. She
has type 2 diabetes mellitus. Her recent HbA1c is 44 mmol/mol (<42). Eye
examination show no evidence of retinopathy.
Her blood pressure is 140/90
mmHg. Her BMI is 32 kg/m2. Her urine is frothy. Urinalysis shows significant
proteinuria. Her urine albumin-to-creatinine ratio (ACR) is markedly elevated
at 46 mg/mmol.
What is the most likely cause of the frothy urine in this
patient?
A) Diabetic nephropathy.
B) Hypertensive nephropathy.
C) Membranous nephropathy.
D) Polycystic kidney disease.
E) Acute interstitial nephritis.
• It is not diabetic nephropathy because:
√ The HbA1c is relatively well-controlled.
√ Also, she does not have diabetic retinopathy, which usually occurs before
diabetic nephropathy.
• It is mot hypertensive nephropathy. This is because the blood pressure is not
elevated to a degree that causes nephropathy.
No points in the stem support a diagnosis of Polycystic kidney disease or
acute interstitial nephritis.
• The correct answer here is (B) → Membranous nephropathy.
36
Membranous nephropathy:
• (Thickening of the glomerular basement membrane
• It is the most common cause of idiopathic Nephrotic Syndrome in Adults
(especially > 40 YO).
• Presentation: proteinuria / nephrotic syndrome / chronic kidney disease
• Cause: idiopathic (Mainly), infections, rheumatoid drugs, malignancy
• Prognosis:
♦ 1/3 of the cases → Remission.
♦ 1/3 of the cases → Partial Remission.
♦ 1/3 of the patients → progress into End-stage Renal Failure.
What is the most definitive “diagnostic” investigation?
→ Renal biopsy.
37
Important notes on SGLT2 Inhibitors (Flozin Family):
Sodium-Glucose Co-Transporter-2 inhibitors
• In addition to ACE inhibitors → provide renal, cardio, and diabetic protection.
• Thus, you can add it to ACE inhibitor if needed (eg, if HbA1c is still > 48
mmol/mol).
• SGLT2 inhibitors are beneficial in patients with Type 2 diabetes +
cardiovascular disease/ risk.
• Examples of SGLT2 inhibitors → flozin → Dapagliflozin, Canagliflozin,
Empagliflozin.
38
Scenario
A 55-year-old woman presents to the clinic for a routine follow-up visit. She
has type 2 diabetes mellitus.
Her recent HbA1c is 44 mmol/mol (<42). Eye
examination show no evidence of retinopathy. Her blood pressure is 140/90
mmHg. Her BMI is 32 kg/m2. Her urine is frothy.
Urinalysis shows significant
proteinuria. Her urine albumin-to-creatinine ratio (ACR) is markedly elevated
at 46 mg/mmol.
What is the most likely cause of the frothy urine in this
patient?
A) Diabetic nephropathy.
B) Hypertensive nephropathy.
C) Membranous nephropathy.
D) Polycystic kidney disease.
E) Acute interstitial nephritis.
• It is not diabetic nephropathy because:
√ The HbA1c is relatively well-controlled.
√ Also, she does not have diabetic retinopathy, which usually occurs before
diabetic nephropathy.
• It is mot hypertensive nephropathy. This is because the blood pressure is not
elevated to a degree that causes nephropathy.
No points in the stem support a diagnosis of Polycystic kidney disease or
acute interstitial nephritis.
• The correct answer here is (B) → Membranous nephropathy
40
Mineral Bone Disease
◙ Mineral Bone disease is seen in late-stages chronic kidney disease (stage 4
and above).
◙ Basic problems in chronic kidney disease (CKD):
√ 1-alpha hydroxylation normally occurs in the kidneys
→ CKD leads to low vit D
√ The kidneys normally excrete phosphate → CKD leads to high phosphate.
low vitamin D.
◙ This, in turn, causes other problems:
√ The high phosphate level 'drags' calcium from the bones, resulting in
osteomalacia.
√ Low calcium: due to lack of vitamin D, high phosphate
√ Secondary hyperparathyroidism (↑ PTH): due to low calcium, high
phosphate and low vitamin D.
41
◙ Management: ckd
In the exam, to address -treat- the biomedical abnormalities, pick:
→ Calcium and Vitamin D supplements (eg, AdCal-D3).
The aim of Rx is to reduce phosphate and parathyroid hormone levels.
• Vitamin D or its analogue eg, Alfacalcidol, calcitriol + Calcium supplements.
• Reduced dietary intake of phosphate is the first-line management.
• Phosphate binders: eg, sevelamer (a non-calcium-based binder that is now
increasingly used).
• Parathyroidectomy may be needed in some cases.
42
Scenario:
A patient with CKD that has become a late stage (4 or more) presents with:
↓calcium, ↑phosphate, ↑PTH (secondary not tertiary hyperparathyroidism)
• Think → Mineral Bone Disease.
• What is the type of hyperparathyroidism here (↑PTH)?
→ Secondary hyperparathyroidism (low or N. calcium, high or N. phosphate).
• What is the most likely cause of these blood abnormalities?
→ Vitamin D deficiency.
• Why not tertiary hyperparathyroidism (as it can be cause by end-stage CKD)?
→ In tertiary hyperparathyroidism, calcium would be high (↑) not low as here.
• What is the most appropriate management to address these abnormalities?
→ Calcium and Vitamin D supplements (eg, AdCal-D3).
43
URTI (sore throat, enlarged tonsils). or GE (Gastroenteritis)
1-2 days later presents with hematuria especially in young patients
± Deranged Kidney function tests (with or without).
→ IgA glomerulonephritis (Berger’s disease).
Management (imp):
• If normal blood pressure, low proteinuria (<50 urine protein: creatinine ratio):
→ Supportive Rx (continue to observe). √
• If high blood pressure OR Significant proteinuria (>50 mg/mmol uPCR)
→ ACE inhibitor.
→ Prednisolone • If high proteinuria (> 1g/ day) or (<50 mg/mmol uPCR)
can also be used
44
Ckd and lipid profile
NICE guidelines suggest:
Patient with chronic kidney disease should take lipid modification agents (eg,
atorvastatin).
This is despite their lipid profile results and without the need of a
formal risk assessment.
45
If you suspect Nephrotic Syndrome (a child with facial swelling followed by
total body swelling; ↑ in weight, scrotal edema, LL pitting edema)
urinalysis
The initial step is →
(Urinalysis initially to check for proteinuria and then do more investigation eg,
serum albumin level.
Renal biopsy is diagnostic and in children the most
common type is minimal change nephrotic syndrome).
46
◙ In nephrotic syndrome, remember the triad of:
1. Proteinuria (> 3g/24hr).
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
Other possible findings
→ frothy/ foamy urine, fatigue, ↑ weight, loss of appetite.
47
Nephrotic syndrome
Important:
The anatomical structures affected in nephrotic syndrome are
→ Glomeruli.
Glomeruli are small structures – small blood vessels that filter the blood from
unwanted substances and keep important substances
such as proteins in it.
When damaged as in nephrotic syndrome,
they throw proteins (mainly
albumin) in the urine,
causing proteinuria and hypoalbuminemia and as a
result, oedema.
48
Example:
A 48-year-old diabetic patient presents for review in the GP surgery. Lab test
have been made and compared to his lab results of one year ago.
The eGFR
was 48 a year ago, now it is 22. The other renal function tests are normal.
What is the most appropriate next step?
→ Refer to nephrology.
Here, eGFR has become <30
And also, there is a decline of more than 15 units in 12 months.
49
When should a GP refer a patient to a Nephrologist?
• If eGFR becomes < 30.
• If eGFR declined by ≥ 25% within 12 months + a change of CKD category.
• If eGFR declined by ≥ 15 units within 12 months (sustained ↓).
• If ACR ≥70 mg/mmol (unless diabetic).
50
A 60 YO man with hypertension and overactive bladder is on amlodipine (for
HTN) and oxybutynin (for overactive bladder)
and his BP is still high (150/95).
His creatinine and urea are elevated. His GFR is 38 and his ACR is 40. What
should be done?
→ Add ACE inhibitor (eg, ramipril) or ARBs (eg, losartan).
• We add ACEi to the already being taken amlodipine.
• This is step 2 in managing hypertension (using 2 drugs if 1 drug is not
controlling the hypertension)
• Since he is > 55 YO, he was started on amlodipine; a calcium channel blocker.
However, his HTN is not controlled. Thus, we go to step 2 to by ADDING
another anti-hypertensive, which is ACEi or ARBs.
• Being with chronic kidney disease and proteinuria (ACR > 30) also supports
the addition of ACEi or ARBs as they can slow the deterioration of kidney
functions.
51
A 60 YO man with hypertension and overactive bladder is on amlodipine (for
HTN) and oxybutynin (for overactive bladder) and
his BP is still high (150/95).
His creatinine and urea are elevated. His GFR is 38 and his ACR is 40. What
should be done?
→ Add ACE inhibitor (eg, ramipril) or ARBs (eg, losartan).
(ACEi (eg, ramipril, lisinopril) or ARBs (eg, losartan) are the preferred drug for
Hypertensive patients of any age/ ethnicity with chronic kidney disease as long
as GFR > 30 and
urine Albumin: Creatinine Ratio (ACR) > 30
[They slow the progression of CKD].
√ A ratio of albumin (mcg/L) to creatinine (mg/L) [ACR] of < 30 is normal.
√ A ratio of 30-300 signifies microalbuminuria (proteinuria) and values above
300 are considered as macroalbuminuria. (Albumin is a protein).
52
A 60-year-old man with diabetes mellitus type 2 and hypertension on
metformin and losartan presents complaining of lower limb edema. His urine
is frothy. Fundoscopy is unremarkable (no retinopathy).
His lab results are:
Hemoglobin 121 g/L. (130-180).
Sodium 133 mmol/L (135-146).
Potassium 5.0 mmol/L. (3.5-5.3).
Urea 22 mmol/L (2.5-7.8).
Creatinine 135 mmol/L (45-95)
HbA1c 50 mmol/mol (<48).
Protein:Creatinine ratio 300 mg/mmol (<50).
What is the most likely diagnosis?
A) Diabetic nephropathy. Or:
B) Membranous nephropathy.
• The patient has features of nephrotic syndrome: Edema, proteinuria
(Protein:Creatinine ratio of 300 equals = 3-gram protein in urine in 24 hours).
• The commonest cause for nephrotic syndrome in adults is membranous
nephropathy.
• Also, HbA1c of 50 mmol/mol is not a big number to cause diabetic
nephropathy. This means, his diabetes is controlled!
• Also, there is no retinopathy here, and usually, nephropathy occurs after
retinopathy (however not always, but it a helping hint).
• Also, idiopathic membranous nephropathy is common in diabetic patients.
◙ Therefore, the likely Dx here is → Membranous nephropathy.
53
One of the important complications of CKD is Anemia (eg, extreme fatigue,
sleepiness, pallor). “Due to impaired iron absorption and erythropoietin
production”
◙ In patients with CKD and Anemia but with normal serum Ferritin and iron
Give
→ Erythrocyte stimulating agents. They don’t need iron.
◙ In patients with CKD and Anemia + Low serum Ferritin/ iron
Give → Iron supplements followed by erythrocyte stimulating agents.
54
55
56
Repeated UTI but suddenly developed (loin or back pain, fever, rigors),
[±]
Urinalysis shows blood,
nitrites, leucocyte esterase.
→ ACUTE Pyelonephritis.
57
• Chronic pyelonephritis has no active infection! The symptoms may be 2ry to
renal failure.
When you see Hypertension + Hx of repeated urinary tract infections (UTIs)
→ Think of: CHRONIC Pyelonephritis
Repeated UTIs → Renal Scarring → Chronic Pyelonephritis → Hypertension
58
A pregnant woman presents with fever, rigors, lower abdominal pain, dysuria
and frequency.
The pain was at the lower abdomen then it becomes more
generalised and radiates to the right loin.
→ Acute Pyelonephritis.
Pyelonephritis = inflammation of the pelvis of the kidney (usually due to
Ascending UTI).
• Some RFx →
Pregnancy,
Stones,
Vesico-ureteric reflux (VUR),
DM.
59
60
• Suspect it if
√ Lower UTI features (dysuria -burning or difficult urination, frequency,
urgency, suprapubic (lower abdominal) pain]
√ [+] Fever, Rigors, Loin pain or Back pain
√ [±] Urinalysis → blood, nitrites, leucocyte esterase.
Acute pyelonephritis
61
√ Dysuria, frequency, urgency ± lower abdominal Pain →
Lower uti
(or) → Trimethoprim Nitrofurantoin
62
√ The above + Loin or Back pain + fever
Dysuria, frequency, urgency ± lower abdominal Pain →
√ The above + Loin or Back pain + fever → Acute pyelonephritis (Upper UTI)
→ Ciprofloxacin (or) Co-amoxiclav.
63
◙ Investigations:
UTI
• Do Urinalysis → to look for (blood, protein, nitrate, leucocyte esterase).
• Do before commencing empirical antibiotics.
√ (midstream specimen for adult and old children)
√ (sometimes in young children → clean catch or via catheter or even via
suprapubic aspiration).
64
♦ Important,
the most common causative organism of UTI → E. coli (Gram -ve).
◙ Treatment (often requires admission)
Antibiotic lines differ from hospital to another; however
, the following
regimens are advised by NICE:
Start empirical Antibiotics immediately.
Important, in Acute pyelonephritis, once the urine sample for culture and
sensitivity has been sent
→ The empirical antibiotics may need to be changed after the culture results.
65
Ciprofloxacin: 500 mg BID for 7
days. [or]:
√ Co-amoxiclav 625 mg TID for 14
days.
BID: Twice a day ▐ TID: 3 times a day.
• Non-pregnant women
• Men
• Patients with indwelling catheters
66
Children
√ 1st line → Co-amoxiclav.
√ 2nd line → Cefixime.
67
Pregnant ♀ who does not require
admission
Cefalexin (PO) 500 mg BID for 10-14
days. “important √
68
UTI RX
”
If the patient is admitted, these antibiotics are given Intravenously “IV”.
In short:
• Acute pyelonephritis → Urine analysis + Urine Culture → Then Start Antibiotics.
• Lower UTI → Trimethoprim (or) Nitrofurantoin.
• Upper UTI → Ciprofloxacin (or) Co-amoxiclav.
• Pregnant → Cefalexin.
69
Quick info:
√ Small Kidneys + Hypertension
Think → Bilateral renal artery stenosis [OR] Chronic Pyelonephritis.
√ ACE inhibitors are contraindicated in Bilateral Renal artery stenosis.
(see Vascular chapter).
70
• It is sometimes normal to find mild proteinuria on urine dipstick (traces up to
+1) especially in those who regularly exercise such as gym attendees.
• If no symptoms and they are healthy regardless of the mild proteinuria
→ Repeat the test.
• If still high
→ Do 24-hour urine specimen test or Protein Creatinine Ratio.
• Never refer a patient with an “isolated proteinuria” to a Renal Clinic.
As a GP, you need to investigate further.
71
Nephrotic Syndrome
◙ Around 80% of cases in children are due to Minimal change glomerulonephritis.
Note that microscopic hematuria can be seen in 10-30% in minimal change disease.
◙ Minimal change disease almost always presents as nephrotic syndrome,
accounting for
75% of cases in children
and 25% in adults.
◙ The condition generally carries a good prognosis with around 90% of cases
responding to high-dose oral steroids.
◙ Other features include hyperlipidaemia,
hypercoagulable state (due to loss
of antithrombin III)
and liability to infections
(due to loss of immunoglobulins).
◙ Triad of:
1. Proteinuria (> 3g/24hr).
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
◙ In children, the peak incidence is between 2 and 5 years of age.
72
◙ Features of minimal Change glomerulonephritis:
√ Nephrotic syndrome.
√ Normotension – hypertension is rare.
√ Selective proteinuria (only intermediate-sized proteins such as albumin
and
transferrin can leak through the glomeruli).
(The Definitive Diagnostic Test)
√ Renal biopsy
Electron microscopy shows fusion of podocytes.
73
Example (1),
A 5 YO child presents with ↑ weight, Puffy eyes, Lower limb swelling.
He is
otherwise healthy and happy. Urine Dipstick reveals +3 Proteinuria.
What is the next best step?
We suspect Nephrotic Syndrome. 2 of the triad are given;
Proteinuria and
Oedema (puffy eyes, swelling, increase weight). So, to diagnose it, request
→ Serum albumin levels. (to complete the aforementioned Triad).
Another valid answer → → Urine protein to creatinine ratio.
Once diagnosed, we can refer to renal clinics.
74
What is the best diagnostic test? For nephrotic syndrome
→ Renal Biopsy. (Electron microscopy → fusion of podocytes).
75
Example (2),
2 YO child was noticed by his mother to be gaining weight regardless of his
poor feeding.
There is gradual swelling of his face, feet and legs.
The child feels
fatigued, and his urine is noted to be foamy.
The likely Dx → Nephrotic Syndrome.
The most appropriate Investigation → Another valid answer → → 24-Hours urinary protein.
Urine protein to creatinine ratio.
Remember, Nephrotic Syndrome = Proteinuria + Albuminemia + Oedema.
Thus, 24-hour protein in urine diagnosis in this case as he already had oedema manifested.
+ serum albumin levels are required to help in
• Note, one important explanation of foamy urine is the presence of high
protein in it.
76
77
Example (3),
40 YO ♂ known hypertensive presents with tiredness, lethargy, fluid retention
and proteinuria.
His serum albumin is found to be low.
• In the exam, always definitive diagnostic test”.
In Nephrotic syndrome, _____is definitive
as it can show the exact etiology.
The most “Definitive” diagnostic test → Renal Biopsy (it shows the etiology).
• This patient has proteinuria, albuminemia and fluid retention (swelling) →
the triad of Nephrotic Syndrome.
78
Example (4),
6 YO child presents with progressively increasing swelling of his face, scrotum
and legs.
His urine is frothy. Renal biopsy shows no abnormalities on light
microscopy.
However, electron microscopy reveals abnormal fused podocytes.
The likely Dx → Minimal change disease.
79
Example (5),
5 YO child presented a week ago with progressively increasing swelling of his
face, scrotum and legs and with frothy urine.
Renal biopsy confirmed the Dx of
Nephrotic syndrome and accordingly the patient was started on steroids.
He
presents now with flank pain, hematuria and fluctuating urea levels.
A
diagnosis of renal vein thrombosis is made. What is the most likely cause for
this renal vein thrombosis?
→ Antithrombin III deficiency
√ Remember that proteinuria is one of the triad of Nephrotic Syndrome.
√ Proteinuria means loss of proteins in urine such as albumin and anti-
coagulation factors including Anti-thrombin III.
√ Loss of Antithrombin III → ↑ Coagulation (↑ Thrombosis).
√ Rx → Anti-coagulation.
80
• Prolonged vomiting and diarrhea can lead to →
Dehydration, Hypokalemia (↓ K).
• Dehydration “Hypovolemia” can lead to → Acute Kidney Injury (AKI)
.
• Prerenal causes “Especially hypovolemia” is the most common cause of AKI.
• Once there is AKI →
↓ eGFR → Kidneys are unable to well execrate
Potassium, Creatinine, Urea…etc. →
Hyperkalemia, ↑ serum urea and
Creatinine.
81
CT scan with contrast, to reduce the risk of “Contrast Induced
Nephropathy”
→ Drink Plenty of Fluids.
Another correct answer is
→ IV fluid normal saline (0.9% NaCl) pre and post procedure especially in high
risk patients such as elderly with DM.
• Additional Note, metformin is Nephron-harmful and thus needs to be ceased
“stopped” before any contrast study.
82
The steps (approach) to determine the type of the blood gas
abnormality.
1. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)?
2. Respiratory component: What has happened to the PaCO2?
83
Respiratory component: What has happened to the PaCO2?
• PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory
compensation for a metabolic alkalosis)
• PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory
compensation for a metabolic acidosis)
84
3. Metabolic component: What is the bicarbonate level/base excess?
• bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a
metabolic acidosis (or renal compensation for a respiratory alkalosis)
• bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)
suggests a
metabolic alkalosis (or renal compensation for a respiratory acidosis)
Simply, know that CO2 is an Acid, and Bicarbonate (HCO3) is an Alkali.
85
Example (1):
pH 7.17 (Normal: 7.35-7.45)
PCO2 2.5 (Normal: 4.7-6 kPa)
Base excess -14 (Normal -2 to +2)
→ Metabolic acidosis (with partial respiratory compensation).
♦ As the pH < 7.35 → definitely Acidosis.
♦ PCO2 (the acid) is low → this is compensation by the lungs; they try to
breathe quickly to get rid of the CO2 (the acid) to buffer the acidity.
The
patient might present with tachypnea or SOB.
♦ Base excess is very low → metabolic acidosis.
86
Example (2):
An elderly man was found on the floor unconscious by his neighbours. The
ambulance crew came. His Systolic BP was 65mmHg. He was resuscitated in
the ambulances (given 1.5 L NaCl 0.9%). He was further resuscitated in the
emergency department. He mentions that he had severe diarrhea over the last
2 days.
His labs show:
pH 7.18 ▐ Base excess -13 ▐ Lactic acid 6 (high)
Urea and Creatinine are high ▐ CRP 160 (high)
His blood gas interpretation → Metabolic Acidosis
As his pH < 7.35 → Acidosis
His Base excess is very low (< -2) → Metabolic Acidosis.
This patient had profuse diarrhea for 2 days. Remember that profuse
diarrhea can lead to loss of HCO3 “Bicarbonate” and thus metabolic acidosis.
Also, remember that profuse diarrhea can lead to → Hypovolemia
“Dehydration”, which is an important prerenal cause for AKI. That’s why his
renal functions are impaired.
Also, once AKI develops → ↓ eGFR → accumulation of K+ and others.
(Hyperkalemia).
87
Managing Renal Stones (also in urology section)
Generally, the Stone Size Rule:
◙ If stone size <______→ ↑ fluid intake to get rid of it in urine.
◙ If stone size _____cm → two options:
√ ESWL (Extracorporeal Shock wave Lithotripsy) “preferred”, or:
√ Ureteroscopy with dormia basket.
◙ If stone size _____→ Percutaneous Nephrolithotomy.
Managing Renal Stones (also in urology section)
Generally, the Stone Size Rule:
◙ If stone size < 0.5 cm (< 5 mm) → ↑ fluid intake to get rid of it in urine.
◙ If stone size 0.5 cm – 2 cm → two options:
√ ESWL (Extracorporeal Shock wave Lithotripsy) “preferred”, or:
√ Ureteroscopy with dormia basket.
◙ If stone size > 2 cm → Percutaneous Nephrolithotomy.
88
89
HOWEVER!
◙ If the patient has only one functioning kidney (e.g. Hx of the removal of one
kidney) and
has a stone (OF ANY SIZE) with dilatation of the pelvicalyceal
system (PCS) ±
Anuria, Fever [Obstructive Uropathy
] →
The This is done by → thing to do is to decompress the PCS to save the remaining kidney.
Percutaneous Nephrostomy
INITIAL ◙ Similarly, even if the patient has 2 kidneys, if he develops
AKI (impaired urea
and creatinine),
fever and Hydronephrosis (these together with
the presence
of stones are indicative of Obstructive Uropathy),
we shall go for
(Percutaneous Nephrostomy)
in order to temporarily and instantly
decompress the renal collecting system regardless of the stone size!
Note, Percutaneous nephrostomy is different form Percutaneous
nephrolithotomy.
• Percutaneous Nephrostomy → stoma “catheter” to the Pelvicalyceal system
of the kidney for decompression (Draining the obstructed fluid in kidney).
→ removal of urinary stone percutaneously
• Percutaneous Nephrolithotomy
via a scope (if size > 2 cm).
90
91
Example (1),
46 YO ♂ with Hx of left nephrectomy 10 days ago presents with fever, inability
to pass urine for the last 20 hours.
Ultrasound reveals an 8 mm stone in the
left lower ureter with dilatation of the pelvicalyceal system. What is the best
INITIAL step in management?
• The best initial step → Percutaneous Nephrostomy.
The (Stone Size Rule) does not apply here. This patient has obstructive
uropathy with impending renal failure.
We need to, initially, save his
remaining kidney by decompressing the fluid retention in the PCS.
This can be
done by → Percutaneous Nephrostomy. Afterwards, we can manage the stone
based on the stone size role; (ESWL) in this case.
92
Renal stone management based in symptoms
In summary:
◙ Loin pain + Stone ± Hydronephrosis → Manage according to the stone size.
◙ Loin pain + Stone + Hydronephrosis [+] AKI [+] Fever
→ Percutaneous Nephrostomy.
93
Example (2),
36 YO ♂ presents with severe loin pain, nausea and vomiting.
Ultrasound
shows right hydronephrosis. Non-enhancing CT reveals a 3.1 cm stone
The most appropriate management → Percutaneous Nephrolithotomy.
He has 2 working kidneys with no AKI. According to the “Stone Size Rule”,
stone > 2 cm → Percutaneous Nephrolithotomy.
If there was AKI with fever, the “initial” step would be to decompress the PCS
by percutaneous nephrostomy.
We hope the concept is clear.
94
Hypertensive patient with CKD “Chronic Kidney Disease” with GFR is still > 30
and ACR is > 30.
→ Give ACE inhibitors (e.g., ramipril, lisinopril) to manage HTN or ARBs.
[They slow the progression of CKD].
However, avoid ACEi and ARBs if GFR < 30 or ACR < 30 in patients with HTN.
(ACEi (eg, ramipril, lisinopril) or ARBs (eg, losartan) are the preferred drug for
Hypertensive patients of any age/ ethnicity with chronic kidney disease as
long as GFR > 30 and Albumin: Creatinine Ratio (ACR) > 30
◙ Also, remember: DM type 2 + HTN → always consider ACEi (it is
reno-protective) unless severe renal impairment (GFR < 30).
95
◙ ACEi and ARBs can be used to delay the progression of end stage renal
failure. They can be used in the following situations (as long as):
• ACR ≥ 70 (ACR = urinary Albumin: Creatinine ratio).
• ACR ≥ 30 (If there is HTN).
• ACR ≥ 3 (If there is DM).
96
◙ Important notes:
• In addition to ACE inhibitors → _______provide renal, cardio, and diabetic protection.
• Thus, you can add it to ACE inhibitor if needed (eg, if HbA1c is still > 48
mmol/mol).
• SGLT2 inhibitors are beneficial in patients with Type 2 diabetes +
cardiovascular disease/ risk.
• Examples of SGLT2 inhibitors →
◙ Important notes:
• In addition to ACE inhibitors → provide renal, cardio, and diabetic protection.
• Thus, you can add it to ACE inhibitor if needed (eg, if HbA1c is still > 48
mmol/mol).
• SGLT2 inhibitors are beneficial in patients with Type 2 diabetes +
cardiovascular disease/ risk.
• Examples of SGLT2 inhibitors → flozin → Dapagliflozin, Canagliflozin,
Empagliflozin.
97
◙ The most common cause of Nephrotic Syndrome in Children
→ Minimal Change Glomerulonephritis.
◙ The most common cause of Nephrotic Syndrome in Adults:
√ in Caucasian ▐ White people ▐ or if unspecified ethnicity → membranous GN
√ in Africans ▐ Black ▐ Americans ▐ Hispanics → Focal Segmental GN.
Generally, for PLAB 1, the most common cause of Nephrotic Syndrome in
Adults (especially > 40 YO) → Membranous GN
98
Membranous GN
Membranous glomerulonephritis
• Presentation:
proteinuria
/ nephrotic syndrome
/ chronic kidney disease
• Cause: idiopathic (Mainly),
infections,
rheumatoid drugs,
malignancy
• Prognosis:
♦ 1/3 of the cases → Remission.
♦ 1/3 of the cases → Partial Remission.
♦ 1/3 of the patients → progress into End-stage Renal Failure. No
99
Nephrotic and nephritic
Types of Glomerulonephritis “For Reading”
There are 2 Main types
1) Presents with Nephritic syndrome: eg, rapidly progressive (Goodpasture), IgA
2) Presents with Nephrotic Syndrome: eg, minimal change, membranous, focal seg.
100
101
◙ Typically presents with Nephritic Syndrome (haematuria, hypertension):
♣ Rapidly progressive glomerulonephritis (Crescentic glomerulonephritis):
√ Rapid onset, often presenting as acute kidney injury.
√ Causes include
Goodpasture’s (hematuria + Hemoptysis),
ANCA positive vasculitis.
♣ IgA nephropathy (Berger’s disease) and Mesangioproliferative GN:
√ Typically, young adult with haematuria 1-2 days after a URTI or less often after
gastroenteritis.
102
Typically presents with Nephrotic Syndrome (proteinuria, oedema):
♣ Minimal change disease:
√ Typically, a child with nephrotic syndrome (Edema, proteinuria, albuminemia)
• Minimal change disease accounts for 80% of Nephrotic Syndrome cases in children.
√ Causes: Idiopathic (mainly),
Hodgkin’s, NSAIDs
√ Good response to steroids
√ Renal biopsy on electron microscopy → Fusion of Podocytes.
103
Typically presents with Nephrotic Syndrome (proteinuria, oedema):
♣ Membranous glomerulonephritis:
√ Presentation:
proteinuria /
nephrotic syndrome /
chronic kidney disease.
√ Cause:
idiopathic (mainly),
infections,
rheumatoid drugs,
malignancy.
√ 1/3 resolve,
1/3 respond to cytotoxics,
1/3 develop chronic kidney disease.
104
Typically presents with Nephrotic Syndrome (proteinuria, oedema):
♣ Focal segmental glomerulosclerosis
√ May be idiopathic
or secondary to HIV,
heroin.
√ presentation: proteinuria
/ nephrotic syndrome
/ chronic kidney disease.
105
106
107
Anemia + Hypocalcemia and Hyperphosphatemia + Small Kidneys on U/S (< 9 mm).
◙ Patients with late CKD usually have Hypocalcemia which results in tingling,
numbness, paraesthesia, involuntary spasms/ cramps.
◙ The reason for this Hypocalcemia is:
25-hydroxyvitamin D is formed in liver → Then, an enzyme called (1-alpha-
hydroxylase) in kidneys converts it to the active form → 1,25-dihydroxyvitamin D.
In CKD → deficiency of 1-alpha hydroxylase → ↓ vit D and calcium.
108
Example,
An elderly patient with CKD and DM presents with loss of sensation in his
fingers and muscle cramps.
His labs show:
Hyperkalemia, Hypocalcemia, hyperphosphatemia, and Anemia.
◙ The likely reason for his symptoms is → Hypocalcemia
◙ IMPORTANT & TRICKY: Sometimes the answer would be indirect, such
as → 1,25-dihydroxyvitamin D3 deficiency. “the active form of Vit. D”.
◙ Another valid answer: Sometimes the answer would be indirect, such as
→ 1,25-dihydroxycholecalciferol overreplacement. “
√ In end stage kidney disease → ↓ Vitamin D → ↓ calcium → The body will try
to compensate for this hypocalcemia →
↑ bone turnover rate (and ↑
parathyroid hormone to increase the reduced calcium)
→ with time, as PTH ↑,
Ca also ↑,
and this suppresses the PTH making it back to normal
. It also
suppresses the elevated bone turnover leading to → reduced bone turnover
√ reduced bone turnover also called adynamic bone disease which causes
musculoskeletal pain and immobility.
In adynamic bone disease due to 1,25-
dihydroxycholecalciferol overreplacement,
there will be hypocalcemia +
inappropriately normal PTH.
1,25-dihydroxyvitamin D3 deficiency → ↓ Calcium absorption → Hypocalcemia
Be careful, the question asks about the “cause” for his symptoms, which is
hypocalcemia
2ry to 1,25-dihydroxyvitamin D3 deficiency in this stem.
109
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
If a patient presents with Hematuria (either microscopic or gross)
[+] HTN
[+]
Loin/Flank Pain.
→ think of Adult Polycystic Kidney Disease (ADPKD. “
Important √”
• Remember that ADPKD is associated with Intracranial Aneurysm! (Important √)
110
Example,
A 44 YO ♀ Known cases of Chronic Kidney Disease presents with Hypertension
and loin pain.
Her father died at the age of 54 due to cerebral aneurysm.
What
is the likely Investigation that would lead to diagnosis in this lady?
→ Ultrasound of the Kidneys, Ureters and Bladder.
√ You supposed to be able to know that this is a case of ADPKD as this disease
is an Autosomal dominant which means
that 50% of children will be affected
(Hx of father) and it is often associated with intracranial aneurysm.
√ Furthermore, ADPKD can lead to progressive CKD.
√ The diagnosis is made by as it can detect the cysts.
111
Hematuria + Bloody diarrhoea
Hemolytic Uremic Syndrome (HUS)
(E.coli)
112
Hematuria + Hemoptysis
+ Nasal/Sinus problems
Wegener’s (Granulomatosis with polyangitis)
c-ANCA
113
Hematuria + Hemoptysis Anti-GBM Abs
Good pasture syndrome
114
Hemolytic Uremic Syndrome (HUS)
Triad:
1) Hemolytic Anemia (Hemolysis)
2) Uremia (Acute Renal Failure): low urea and creatinine.
3) Thrombocytopenia (Low Platelets)
♦ Children
115
Eating Undercooked Contaminated food → E. Coli O157 → Produce Verotoxin
→ Profuse Diarrhea → turns to Bloody Diarrhea → (after 2-14 days)
→ Uremia
“Acute Renal Failure” (Hematuria, Proteinuria, ↑ Urea and Creatinine)
So, remember:
• Diarrhea
→ turns Bloody
→ Renal Failure (namely: (Hematuria, high Creatinine…etc).
Acute kidney injury) √
± Features of Anemia (e.g. Pallor, Fatigue
).
Rx → Supportive:
√ IV fluids. √ ± Blood Transfusion √ ± Dialysis (if required)
√ If Very Severe → Plasma Exchange
◙ Never Give Antibiotics in HUS!
(More toxins are released as the E. Coli dies)
116
HUS Triad [+] Fever [+] Neurological manifestations
TTP “Thrombotic Thrombocytopenic Purpura”
117
Hematuria that develops after a Hx of Upper Respiratory Tract
Infection (URTI) (Sore throat/ Coryza)
or less often after
gastroenteritis is either due to either:
♦ IgA Glomerulonephritis (Berger’s Disease) [OR]
♦ Post-Streptococcal Glomerulonephritis.
118
Organism → Group A beta-hemolytic Streptococci (usually Streptococcus Pyogenes)
√ Treatment → Mainly Supportive √ (the Majority resolves spontaneously).
Post-Streptococcal
Glomerulonephritis
1-2 weeks after URTI
♦ Associated with ↓ Complement levels (C3).
♦ Renal biopsy → “Humps” on electron
microscopy.
Main Presentation → Proteinuria
119
(Berger’s Disease)
IgA Glomerulonephritis
IgA Glomerulonephritis
1-2 days after URTI
Main presentation → Hematuria.
Usually Young Males
120
Causes of Small Kidneys:
√ Chronic Pyelonephritis.
√ Chronic Glomerulonephritis.
√ Hypertensive Renal Disease.
√ Bilateral Renal Artery Stenosis
121
Causes of Large Kidneys:
√ ADPKD. (Multiple cysts make kidneys larger)
√ Obstructive Uropathy (e.g. due to stone, enlarged prostate →
Hydronephrosis → large kidney).
122
An elderly patient presents with Nausea and Prostatism (Urinary Frequency,
Hesitancy, Post-void dribbling).
He has HTN. U/S reveals small kidneys. His
serum creatinine is 170 (elevated).
→ Hypertensive renal disease.
Hypertensive renal disease → small and scarred kidneys → Renal
impairment.
123
Large kidneys
√ Large Prostate e.g. Prostate cancer or Benign prostatic hyperplasia (BPH) →
Features of (one of
the causes of Large Not small kidneys. Thus, invalid answer here).
prostatism + Obstructive Uropathy and Hydronephrosis
√ Reflux Nephropathy → Dilated Pelvicalyceal system and occurs mainly in the
young. (Large kidneys).
124
Upper And lower uti
Again
• Simple lower UTI (Dysuria, Frequency) is treated by
→ Trimethoprim or Nitrofurantoin
Regardless of Hx of Hypertension!
• Uncomplicated Upper UTI (Acute Pyelonephritis)
→ Ciprofloxacin or Co-amoxiclav
or Cefalexin (if pregnant + outpatient)
125
A 47 YO ♂ with end-stage chronic kidney disease has had a successful renal
transplant.
Three days later while still in the renal ward, he develops rapid and
shallow breathing, generalised oedema and he is unable to void “anuria”.
His
Vitals and labs are as follows:
HR: 118 bpm ▐ BP: 182/90 ▐ RR: 24
Sodium 136 (N: 135-145) ▐ Potassium 6.6 (N: 3.5-5) ▐ Creatinine 700 (N: 70-150)
The BEST management is → Haemodialysis.
• This is a likely case of Transplant Rejection or Host-Versus-Graft.
• Careful! Many may choose Calcium gluconate or Calcium chloride “to protect
the heart” followed by Insulin and Glucose “to decrease the serum
potassium”. This is NOT the “BEST” management here “the question asks
about the best treatment!”.
• The patient has Severe hyperkalemia + Anuria + Oedema +
Hyperventilation.
• The patient has also Acidosis (indicated by the rapid shallow breathing).
• Lowering the potassium alone would not treat all these features!
• Moreover, the potassium will return to the serum causing hyperkalemia
again. “The patient has no functioning kidney and toxins are accumulating in
his body”.
• Additionally, the patient is already overloaded “generalised edema” with
Anuria “cannot pass urine”; thus, we cannot give him IV fluid!
• Haemodialysis is supportive while we wait for another suitable kidney
transplant.
• K+ ≥ 6.5 → Severe Hyperkalemia.
• Final tip → Calcium Chloride is mainly “but not only” given if there are ECG
changes 2ry to hyperkalemia such as Tall Tented “T” wave, Wide QRS
complex.
126
Some Indications of Hemodialysis:
√ Persistently high potassium ≥ 6.5 [Refractory Hyperkalemia].
√ Severe Metabolic Acidosis.
√ Fluid overloaded with Anuria or non-effective diuretics.
√ Uremic Pericarditis, Pulmonary edema.
√ Uremic Encephalopathy
127
128
Scenario
52 YO man presents to the A&E with fever, rigors and vomiting for 2 days.
There is severe tenderness over the right costovertebral angle.
His Urinalysis is
positive for blood, nitrites and leucocyte esterase.
Creatinine: Normal ▐ Urea: 10 (high) ▐ WBCs: High ▐ CRP: High ▐ K+: Normal.
He was immediately commenced on IV antibiotics and IV fluid.
.
The most appropriate Investigation → Urine Culture and sensitivity. NOT U/S.
• This is likely a case of Acute Pyelonephritis.
• Remember: (loin/ back pain, fever, rigors), [±] Urinalysis shows blood,
nitrites, leucocyte esterase → Acute Pyelonephritis.
129
Pyelonephritis
Here, the question mentions “Costovertebral angle tenderness” instead of
“Loin, back or Flank pain”.
They are nearly the same as the costovertebral
angle is at the (back, towards the flank).
• The investigations for Acute Pyelonephritis are: Urinalysis → then, Urine
Culture.
• It is preferred to take the urine sample for culture before starting the IV
antibiotics. Nonetheless, they have started the antibiotic before the culture in
this stem.
• Remember, in suspicious meningitis, we start empirical IV antibiotics even
before LP or blood culture.
130
Middle aged man with 2 episodes of microalbuminuria. BP 128/70 mmHg.
Normal renal functions
. He is overweight. What additional therapy would
benefit this patient?
a. ace inhibitors
b. Statins
c. B-blockers
d. diuretics
ACE inhibitors are reno-protective (i.e. they delay the progress of CKD)
131
A 5-year-old girl with 5 days history of bloody diarrhoea and dehydration.
Blood culture shows E. coli
Na+ low, K+ high, Creatinine high, Urea high, Calcium Normal, Bicarbonate
low. What is the like diagnosis?
Acute kidney injury
a. b. Addison’s
c. Renal tubular acidosis
√ This is a classic case of HUS (Hemolytic-Uremic Syndrome).
√ HUS is the most common cause of acute kidney injury in children and is
increasingly recognized in adults
132
A 4-year-old boy with recurrent UTI. What is the most likely anatomical
abnormality?
A. VUR
B. Urethral valve
C. Horse shoe kidney
D. Bladder cancer
A
133
5-year-old Girl with recurrent UTI (has had 3 UTIs) responsive to antibiotics.
Next Investigation of choice?
a. MCUG
b. Renal Uss
c. DMSA
d. Urine mcs
e. CTSCAN
B
134
Reflux Nephropathy
• Urine goes back from bladder to ureters and kidneys (Vesico-Ureteric Reflux) →
Dilated Pelvicalyceal system → Repeated UTIs
→ Progressive Renal Failure.
• Occurs mainly in the young (children).
An important cause → Congenital abnormality of the insertion of ureters
into the urinary bladder (can be seen on US).
♦ Dx
√Initial
√Gold standard
1 → Renal Ultrasound (+) Urinalysis, urine culture and sensitivity.
2 → Micturating Cystourethrogram.
√For parenchymal damage (cortical scars) → Technetium Scan (DMSA).
♦ Rx
√ Initially → Low-dose antibiotics prophylaxis (trimethoprim) daily.
√ Failed? Or Parenchymal damage? → Surgery (Ureters Re-implantation).
135
136
A 5 YO child presents with ↑ weight, Puffy eyes, Lower limb swelling.
He is
otherwise healthy and happy. What is the DEFINITIVE diagnostic modality?
→ Renal Biopsy
In Nephrotic Syndrome:
√ Renal biopsy (Definitive Test) → electron microscopy shows fusion of
podocytes.
137
A 69yr old present to emergency department with thirst, anorexia &
lethargy.
He is a known hypertensive not on regular medication or follow up.
OE, blood pressure was 170/100, Urea-high, Creatinine- high, USG shows
bilateral small kidneys.
What is the most likely cause?
Hypertensive nephropathy
138
Large and small kidneys causes
Causes of Small Kidneys:
√ Chronic Pyelonephritis.
√ Chronic Glomerulonephritis.
√ Hypertensive Renal Disease.
√ Bilateral Renal Artery Stenosis.
Causes of Large Kidneys:
√ ADPKD. (Multiple cysts make kidneys larger)
√ Obstructive Uropathy (e.g. due to stone, enlarged prostate →
Hydronephrosis → large kidney).
139
Example,
An elderly patient presents with Nausea and Prostatism (Urinary Frequency,
Hesitancy, Post-void dribbling).
He has HTN. U/S reveals small kidneys. His
serum creatinine is 170 (elevated).
→ Hypertensive renal disease.
Hypertensive renal disease → small and scarred kidneys → Renal
impairment.
140
141
Important,
When you see Hypertension + Hx of repeated urinary tract infections (UTIs)
→ Think of: CHRONIC Pyelonephritis
Repeated UTIs → Renal Scarring → Chronic Pyelonephritis → Hypertension
142
15yr old with facial & ankle swelling. Urinalysis shows protein +++. What is
the likely cause?
Minimal change GN
A.
B. Membranous GN
C. Post streptococcal GN
D. Ig A nephropathy
Minimal change disease
◙ Minimal change disease nearly always presents as nephrotic syndrome,
accounting for 75% of cases in children and 25% in adults.
◙ Around 80% of cases in children are due to Minimal change glomerulonephritis
The condition generally carries a good prognosis with around 90% of cases
responding to high-dose oral steroids.
143
A patient going for CT Scan with contrast. How can you reduce contrast renal
injury?
→ IV Fluids (0.9% Normal saline).
In CT scan with contrast, to reduce the risk of “Contrast Induced
Nephropathy”
→ Drink Plenty of Fluids.
IV fluid normal saline (0.9% NaCl)
Another correct answer → procedure is especially in high risk patients such as elderly with DM.
pre and post
• Additional Note, metformin is Nephron-harmful and thus needs to be ceased
“stopped” before any contrast study.
144
An elderly patient with CKD (Chronic Kidney Disease) and DM presents with
loss of sensation in his fingers and muscle cramps.
His labs show:
Hyperkalemia, Hypocalcemia, hyperphosphatemia, and Anemia.
◙ The likely reason for his hypocalcemia is
→ 1,25-dihydroxyvitamin D3 deficiency. “the more active form of Vit. D”.
◙ Patients with late CKD usually have Hypocalcemia which results in tingling,
numbness, paraesthesia, involuntary spasms/ cramps.
◙ The reason for this Hypocalcemia:
25-hydroxyvitamin D is formed in liver → Then, an enzyme called (1-alpha-
hydroxylase) in kidneys converts it to the active form → 1,25-dihydroxyvitamin D.
Patients with CKD may lack this enzyme and therefore, this conversion does not
occur.
1,25-dihydroxyvitamin D3 deficiency → ↓ Calcium absorption → Hypocalcemia
145
VIT D hydroxyl action
√ 25-alpha-hydroxylation of vit. D occurs in → Liver.
√ 1-alpha-hydroxylation of vit. D occurs in → Kidney.
25-hydroxyvitamin D is formed in liver
→ Then, an enzyme called (1-alpha-
hydroxylase) in kidneys converts it to the active form
→ 1,25-dihydroxyvitamin D.
146
147
So, why is there vitamin D deficiency in chronic renal failure?
→ due to reduced activity of 1-alpha-hydroxylation.
Mnemonic
(K) before (L) in alphabetics.
(1) before (25)
Kidney → 1 ▐ Liver → (25)
Another mnemonic
1K
1=Kid
148
7-year-old boy with increased weight and bilateral swollen legs. No other
complains. Next diagnostic investigation?
A. TFT
B. X-ray
C. Blood glucose
D. Urinalysis
E. LFT
He likely has Nephrotic Syndrome. We need to see protein in urine. So,
urinalysis is the right answer.
Remember, Nephrotic Syndrome = Proteinuria + Albuminemia + Oedema.
Thus, 24-hour protein in urine (Urinalysis) required to help in diagnosis.
+ serum albumin levels are
The most definitive Dx → Renal Biopsy
149
A 23-year-old man was found lying on the floor behind his flat. He is a known
intravenous drug user and has not been seen for 3 days.
Results of his
investigation are as follows: Urea – 45mmol/L, Creatinine 1200 micromole/L
What in–estigation would confirm the cause of his renal impairment?
A. Abdominal Ultrasound scan
B. Blood cultures
C. Serum creatinine phosphokinase
D. Echocardiograph
E. TFT
C
Rhabdimyolysis
• Common Scenarios and Hints: (Important √)
√ A person was trapped for several hours under a heavy object.
√ A fall followed by a long period of lying on the floor.
√ An elderly with frequent falls presents with Acute kidney injury.
√ IV drug abuser was found on the floor not moving for a long period.
√ Long-distance run (e.g. Marathon runner) “Severe Exertion/ Severe
Dehydration”.
√ Severe Crush injury
√ Exercise-induced rhabdomyolysis (e.g. in athletes)
± Hematuria (Reddish Brown or Tea-coloured urine) (False Positive as the
cause of redness is myoglobulin (which has heme), while RBCs are not found in
urine dipstick)
± Hypotension
± AKI (High urea and Creatinine)
± Very high CK (Creatine Kinase)
150
ECG must be performed as the released potassium from the dying muscles
(hyperkalemia) can be dangerous. If ECG changes suggesting hyperkalemia
(Tall tented T wave, Wide QRS) are found:
→ Protect the heart by giving cacl before anything else!
Myoglobulin is nephrotoxic and thus can lead to Acute Kidney Injury (AKI).
Therefore, rehydration with is an essential initial step. That’s why
Rhabdomyolysis is a medical emergency that you have to be aware of!
151
◙ Important points on Rhabdomyolysis:
√ Main Complications of Rhabdomyolysis → AKI and Hyperkalemia.
√ Initial management → (to try to avoid acute kidney injury).
√ Initial Investigation for management → ECG
√ If Tall T wave, Wide QRS, the initial line → (Creatine Phosphokinase) “it indicates muscle necrosis
give IV calcium chloride/ gluconate.
CPK level √ The best initial test that is specific for Rhabdomyolysis → Urine analysis →
Reddish-brown (Tea-coloured) → Falsely +ve hematuria.
√ To confirm → creatinine phosphokinase √ necrosis”.
√ Other lines of treatment include: Sodium Bicarbonate ▐ Dialysis (in severe cases)
152
A hypertensive patient was commenced on a medication. After that, he
developed proteinuria (+3) and renal function impairment. What is the
causative medication?
Deterioration of Renal function tests after initiation of ACE inhibitor in a
hypertensive patient means that the patient already has → which was responsible for his hypertension.
Artery Stenosis So, ACEIs are contraindicated in bilateral renal artery stenosis.
√ Bilateral Small Kidneys + Hypertension
→ Bilateral renal artery stenosis
→ Or: hypertensive renal disease
153
A female presents with dysuria, loin pain and rigors.
Likely → acute pyelonephritis.
Initial investigation → urinalysis.
Then → urine culture.
154
Hematuria that develops after a Hx of Upper Respiratory Tract
Infection (URTI) (Sore throat/ Coryza) or less often after
gastroenteritis is either due to:
♦ IgA Glomerulonephritis (Berger’s Disease) [OR]
♦ Post-Streptococcal Glomerulonephritis
155
2 YO child was noticed by his mother to be gaining weight regardless of his
poor feeding. There is gradual swelling of his face, feet and legs. The child feels
fatigue and his urine is noted to be foamy.
The likely Dx → Nephrotic Syndrome.
√ The most appropriate Investigation → 24-Hours urinary protein.
The most definitive diagnostic test → Renal Biopsy
Remember, Nephrotic Syndrome = Proteinuria + Albuminemia + Oedema.
Thus, 24-hour protein in urine diagnosis.
+ serum albumin levels are required to help in diagnosis
• Note, one important explanation of foamy urine is the presence of high
protein in it.
156
24 YO man was rescued after crush injury in a car accident. He has dark urine
with impaired creatinine and urea. His BP is 100 mmHg and HR is 125 bpm.
• The likely cause of his renal failure → Myoglobin
A case of Rhabdomyolysis
Myoglobin is reno-toxic.
157
A patient with history of chronic glomerulonephritis and diabetes presents
for check-up. He is on metformin. His BP is 144/91.
His creatinine is 151 (normal: 70-150).
Urea is 7.2 (normal: 2-7).
eGFR is 37 (normal >90)
What medication can delay the progression of his renal impairment?
→ ACE inhibitor (e.g., ramipril, enalapril).
“Reno-protective. However, avoid using it if eGFR is < 30”.
158
There are 4 medications that need to be stopped if a patient presents with
Diarrhea/ Vomiting (Risk of Dehydration and AKI) until symptoms resolve:
Diuretics
ACEE inhibitors
Metformin
NSAIDs
DAMN Drugs
Diuretics e.g. Furosemide, bendroflumethiazide) → (↑ dehydration).
Ace inhibitors
(e.g. enalapril, ramipril) and (Arbs e.g. Losartan) → (AKI).
Metformin → (↑ lactic acidosis in a patient with dehydration).
Nsaids → (AKI)
ARBS Risk of Dehydration (Diarrhea/vomiting) → stop DAMN.
159
160
161
Important causes for AKI “Acute Kidney Injury” to remember:
√ Rhabdomyolysis. (prolonged immobilisation, trapped under a heavy rock…).
√ HUS (usually a child with bloody diarrhea then hematuria and KFTs impairment).
√ Dehydration: diarrhea, vomiting (causes of hypovolemia).
√ Sepsis.
√ Following major surgery.
√ DAMN Drugs: Diuretics, ACEi and ARBS, Metformin, NSAIDs.
162
An elderly man is brough by his son to the GP surgery as he complains
of severe lethargy, nausea, loss of appetite and weight loss. His medical
Hx includes HTN.
His BP is 170/115. His renal function tests found to be
abnormal with high urea and creatinine and GFR of 40.
US of kidneys is
performed and reveals reduced cortical thickness and reduced renal
parenchymal volume of both kidneys. What is the most likely Dx?
→ Hypertensive nephropathy.
Hypertensive Nephropathy
• Renal failure 2ry to HTN. If left untreated → ENKD can develop.
• Features → Fatigue, Nausea, Anorexia, Weight Loss, HTN.
US → Small kidneys (reduced parenchymal volume and cortical thickness
bilaterally).
√ It is important to do US to exclude bilateral renal artery stenosis.
163
All patients with Diabetes + Microalbuminuria should be started on
ACE inhibitor (Angiotensin- Converting Enzyme Inhibitors)
such as
enalapril, lisinopril…etc EVEN IF NORMOTENSIVE.
√ DM can lead to diabetic nephropathy.
√ ACEi is reno-protective and would delay the kidney damage.
164
69yr old present to emergency department with nausea, loss of appetite &
lethargy.
He is a known hypertensive not on regular medication or follow up.
OE, blood pressure was 170/100, Urea-high, Creatinine- high
. He is anaemic
and cachectic. His Ca++ is low, creatinine is high, and PSA is 4.5. What is the
most likely cause?
A. Hypertensive nephropathy
B. BPH
C. Prostate car
D. Chronic Pyelonephritis
E. VUR
• Lethargy, loss of appetite and nausea are seen in hypertensive nephropathy.
• If left untreated, hypertensive nephropathy can lead to end-stage kidney
disease (ESKD).
• Prostate cancer is a distractor here as prostate cancer can cause
hypercalcemia (here it is hypokalemia due to ESKD) and in prostate cancer, PSA
would be very high when the patient reaches the level to be cachectic.
165
60 YO man with stage 4 chronic kidney disease on antihypertensive
medications presents with the following:
BP: 160/100
Urinalysis: Protein 1+, Blood 1+
Urea: 8
Creatinine: 240
eGFR: 25
U/S: reduced renal parenchymal volume, reduced cortical thickness
bilaterally.
What is the most likely diagnosis among the options?
A) Chronic pyelonephritis.
B) Unilateral renal artery stenosis.
C) Glomerulonephritis.
D) Rhabdomyolysis.
E) Acute kidney injury.
The stem mentions “bilateral small kidneys”.
• Options A, B, and C can cause small kidneys. In addition, hypertensive
nephropathy can also cause bilateral small kidneys but not mentioned here.
• Option A (chronic pyelonephritis) is not suitable here as there is no mention
of Hx of recurrent infections and scaring.
• Option B (unilateral renal artery stenosis) can cause “unilateral” small kidney.
Thus, it is wrong.
• The most suitable answer here is option C → Glomerulonephritis.
166
A 23 YO man found to have microscopic haematuria on a routine check-up.
His father has chronic kidney disease and a previous haemorrhagic stroke. His
grandfather on his paternal side dies from intracranial haemorrhage. His BP is
155/105.
The investigation that most likely would lead to a diagnosis is:
→ Ultrasound of kidneys, ureters and bladder (US of KUB).
√ He is likely having autosomal dominant polycystic kidney disease (ADPKD).
√ Hematuria + HTN + Strong FHx of hemorrhagic stroke (remember that
intracranial aneurysm is an important association with ADPKD).
√ IMPORTANT:
ADPKD is diagnosed by (U/S of KUB) not by (Genetic testing) as genetic testing
for ADPKD is particularly difficult to interpret
and we resort to it only if U/S is
negative and the suspicious of ADPKD is high
167
A 48 YO man presents to a renal clinic complaining of frothy urine (ie,
proteinuria) + lower limm oedema. He is diabetic and hypertensive.
His blood
pressure is within normal ranges. His labs:
Urine Protein:Creatinine ratio is 490 (normally < 350 mg/mmol).
HbA1C is 45 (normally < 48 mmol/mol).
What is the most likely cause for his proteinuria?
→ Membranous Nephropathy.
• It is not diabetic nephropathy (his HbA1C is normal. Ie, his DM is controlled).
• It is not hypertensive nephropathy (His BP is normal ie, controlled).
• Low urine protein to creatinine ratio + proteinuria + LL edema → think
Nephrotic syndrome.
168
Nephrotic syndrome
• And the commonest cause for nephrotic syndrome in adults is
Membranous nephropathy.
◙ The most common cause of Nephrotic Syndrome in Adults:
√ in Caucasian ▐ White people ▐ or if unspecified ethnicity → membranous GN
√ in Africans ▐ Black ▐ Americans ▐ Hispanics → Focal Segmental GN.
◙ Generally, for PLAB 1, the most common cause of Nephrotic Syndrome in
Adults (especially > 40 YO) → membranous GN
◙ And in children (80% of nephrotic S) → Minimal change glomerulonephritis.
169
A 70 YO man presents to the A&E complaining of difficulty breathing
especially when lying flat. He has end-stage renal failure and is on
hemodialysis.
However, he has missed the last few hemodialysis
appointments.
His creatine and urea are markedly elevated. His serum
potassium is 7 (normal: 3.5-5 nmol/L). His daily urine output is less than 40
ml (ie, he has anuria).
His chest X-ray shows pulmonary oedema. What is the
most appropriate management?
→ Urgent Haemodialysis.
√ Don’t give furosemide to patients with severe renal impairment + Anuria!
√ This patient with uremia and severe hyperkalemia and fluid overload needs
urgent hemodialysis.
170
Important Summary Points – Nephrology:
◙ Antibiotic intake (eg, for URTI) followed by maculopapular rash +
HEMATURIA + fever + Deranged kidney function tests (KFTs)
→ Acute interstitial nephritis.
171
◙ Massive hemorrhage (eg, during surgery), hypotensive shock, Deranged KFTs
→ Acute tubular necrosis.
172
◙ URTI or GE, 1-2 days later presents with hematuria especially in young
patients + Deranged KFTs.
→ IgA glomerulonephritis (Berger’s disease).
173
◙ URTI or GE, 1-2 weeks later presents with Proteinuria “protein in urine” ±
Hematuria + Deranged KFTs.
→ Post-streptococcal glomerulonephritis.
174
A 60 YO woman presents complaining of blood in urine that she has noticed
today.
She had sore throat last week and was given antibiotics.
She has also
developed maculopapular rash on her trunk. Her body temperature is 37.9.
Urea and creatinine are high.
The most likely Dx → Acute interstitial nephritis.
◙ Allergy (e.g., drug intake followed by rash, fever) + Hematuria + ↑ creatinine.
Think → Acute interstitial nephritis.
175
◙ Massive hemorrhage (e.g., during surgery) and hypotensive shock + High
creatinine
Think → (ATN)
(ATN is the commonest renal cause of acute kidney injury).
Acute Tubular Necrosis
√ “The kidneys need to remain well hydrated/ perfused to avoid acute
“tubular” necrosis”.
√ “Prolonged ischemia → “low perfusion” to kidneys → Dying tubules =
necrosis = Acute tubular necrosis → AKI”
176
A 27 YO woman presents with 1-week complaints of strong desire to
empty her bladder,
lower abdominal discomfort, stinging during urination,
right loin tenderness, fever, rigors.
Urinalysis shows leucocytes and nitrates.
• The most likely Dx → • pyelonephritis
The most appropriate Rx → Co-amoxiclav or Ciprofloxacin.
Summary:
√ Dysuria, frequency, urgency ± lower abdominal Pain → Lower UTI
(or) → Trimethoprim Nitrofurantoin. If pregnant → Cefalexin.
√ The above + Loin or Back pain + fever
→ Acute pyelonephritis (Upper UTI)
→ Ciprofloxacin (or) Co-amoxiclav.
177
Q1) A 27 YO woman presents with 1-week complaints of strong desire to
empty her bladder,
lower abdominal discomfort, stinging during urination
and an increased number of urinations.
She is not sexually active. She is
afebrile. There is no loin pain. Her urinalysis shows leucocytes and nitrates
.
• The most likely Dx → lower uti
• The most appropriate Rx → Lower UTI.
Nitrofurantoin.
178
What if the patient with end-stage kidney disease presents with
musculoskeletal pain and hypocalcemia and low Vitamin D and still high PTH?
This patient is having 2ry hyperparathyroidism (still high PTH to try to increase
the low calcium, i.e., still high bone turnover).
This means he is having high bone turnover and even though PTH is high to try
to elevate the serum calcium
caused by the chronic kidney disease, it still is not
enough to compensate the vitamin D.
The diagnosis here 2ry hyperparathyroidism or vitamin D deficiency.
are correct. This patient would benefit from
→ Vitamin D supplements.
179
Initial Rx for (Hypocalcemia) eg, tingling sensation, low serum calcium:
Esrd
→ Calcium gluconate infusion.
(Remember that end-stage renal failure can cause hypocalcemia. If severe and
left untreated it can cause arrhythmia, cardiac arrest and death).
180
A 75 YO woman presents with severe low back pain and pelvic pain.
She has
end-stage kidney disease, type 2 DM, HTN, and ischemic heart disease and
she is on medications for these diseases. X-ray has been done and showed no
fractures.
Blood tests revealed low serum calcium, high phosphate, and
normal parathyroid hormone. What is the most likely cause for her
presentation
?
→ 1,25 dihydroxycholecalciferol overreplacement.
√ In end stage kidney disease → ↓ Vitamin D → ↓ calcium →
The body will try
to compensate for this hypocalcemia → ↑ bone turnover rate (and ↑
parathyroid hormone to increase the reduced calcium)
→ with time, as PTH ↑,
Ca++ also ↑, and this suppresses the PTH taking it back to normal.
It also
suppresses the elevated bone turnover leading to → reduced bone turnover
√ reduced bone turnover also called adynamic bone disease which causes
musculoskeletal pain and immobility.
In adynamic bone disease due to 1,25-
dihydroxycholecalciferol overreplacement, there will be hypocalcemia +
inappropriately normal PTH.
√ 1,25-dihydroxycholecalciferol is the active form of vitamin D
181
A 23 YO man found to have microscopic haematuria on a routine check-up.
His father has chronic kidney disease and a previous haemorrhagic stroke. His
grandfather on his paternal side dies from intracranial haemorrhage. His BP is
155/105.
The investigation that most likely would lead to a diagnosis is:
→ Ultrasound of kidneys, ureters and bladder (US of KUB).
√ He is likely having autosomal dominant polycystic kidney disease
(ADPKD).
√ Hematuria + HTN + Strong FHx of hemorrhagic stroke (remember that
intracranial aneurysm is an important association with ADPKD).
√ IMPORTANT
ADPKD is diagnosed by (U/S of KUB) not by (Genetic testing) as genetic testing
for ADPKD is particularly difficult to interpret and
we resort to it only if U/S is
negative and the suspicious of ADPKD is high.
182
183
