1
Q
Major Functions of the Urinary System?
A
- Excretion of waste: urea; drugs
- Maintenance of fluid volume &
composition - Regulation of Blood pressure ( via renin)
- Regulation of blood glucose
- Regulation of pH
- Hormone synthesis: erythropoietin
- Vit D metabolism
2
Q
What is a nephron and its major processes?
A
- Functional unit of the kidney
- Filtration—by glomerulus
- Reabsorption by renal tubules
- Secretion by renal tubules
3
Q
What is Urea?
A
by-product of amino acid
digestion
4
Q
What is creatinine?
A
by-product of creatine
phosphate in muscles
5
Q
What is uric acid?
A
by-product of RNA digestion
6
Q
What happens to kidney filtration and waste excretion in progressive kidney damage?
A
There is a loss of kidney filtration and less excretion of wastes.
7
Q
A
8
Q
Which two waste products accumulate in the blood as kidney function declines?
A
Creatinine and urea.
9
Q
What is the term for increased nitrogenous waste (BUN) in the bloodstream?
A
Azotaemia.
10
Q
What specific laboratory finding indicates impaired kidney function due to waste accumulation?
A
Elevated blood urea nitrogen (BUN) and creatinine.
11
Q
What was the previous name for Acute Kidney Injury (AKI)?
A
Acute Renal Failure (ARF).
12
Q
How is AKI defined in terms of kidney function?
A
A sudden and often reversible reduction in kidney function, measured by glomerular filtration rate (GFR).
13
Q
What is the overall mortality range for AKI?
A
10–80%.
14
Q
What is the mortality rate for uncomplicated AKI?
A
Around 10%.
15
Q
What percentage of patients with AKI die, and how does this change with stage 3 AKI?
A
> 20% of AKI patients die; this increases to >35% in stage 3 AKI.
16
Q
According to KDIGO, what serum creatinine increase within 48 hours indicates AKI?
A
17
Q
According to KDIGO, what change in serum creatinine over seven days indicates AKI?
A
An increase to ≥1.5 times baseline.
18
Q
According to KDIGO, what urine output threshold indicates AKI?
A
Less than 0.5 mL/kg/h for at least 6 hours.
19
Q
KDIGO staging of AKI
A
20
Q
What are some risk factors for AKI?
A
- Age
- pre-existiong CKD
- Previous episode of AKI
- Dementia
- HF
- Liver disease
- Diabetes Mellitus
21
Q
AKI Etiology
A
- Prerenal causes = any cause of reduced BF to kidney (40-70%)
- Renal causes = include conditions that affect the glomerulus or tubule (10-50%)
- Post-renal causes = mainly include obstructive causes, which lead to congestion of filtration system loading to shift in filtration driving forces (10-20%)
22
Q
Pre-renal AKI
A
Causes that reduced BF to the kidney
- Tubular and glomerular function tends to stay normal
23
Q
Examples of mechanism of prerenal AKI
A
- Hypovolemia
- Hypotension
- Cardiac failure
- Infection
- Renal artery blockage
24
Q
What is the prognosis of prerenal AKI?
A
- Easily reversed if its possible to identify the specific cause and quickly restore renal perfusion
25
Renal AKI
About 90%.
26
How does recovery from intrinsic renal AKI usually progress, and what may occur if the injury is severe?
27
What types of kidney structures are primarily affected in intrinsic renal AKI?
The glomerulus and tubules.
28
What is the most common cause of acute tubular necrosis (ATN) in intrinsic renal AKI?
29
Which drugs commonly cause acute interstitial nephritis in intrinsic renal AKI?
Beta-lactam antibiotics, penicillins, and NSAIDs.
30
Which autoimmune conditions are linked to acute interstitial nephritis?
Systemic lupus erythematosus (SLE) and IgG-related disease.
31
Which condition involves antibodies targeting the glomerular basement membrane, leading to glomerulonephritis?
Autoimmune conditions such as SLE or post-infectious glomerulonephritis.
32
What are two common causes of intratubular obstruction in intrinsic renal AKI?
Tumor lysis syndrome and toxins such as ethylene glycol.
33
What are the causes of Post Renal AKI
- Obstruction within urinary system DISTAL to kidney due to stones, tumour or prostate enlargement
34
What is the process of Post Renal AKI
Obstruction = urine builds up in the kidney = impaired kidney function
35
What is the prognosis of post renal AKI?
May be reversed by removal of obstruction
36
What primarily drives the pathogenesis of AKI?
The underlying etiology (cause).
37
What are the two main causes of acute tubular necrosis (ATN)?
Ischemia and direct toxins.
38
In acute tubular necrosis, what happens to the brush border of tubular cells before cell death?
Effacement (loss of structure).
39
How does glomerulonephritis cause kidney damage?
Through direct immune-mediated vessel injury or immune complex deposition damaging the glomeruli.
40
What are two examples of intratubular obstructions that reduce tubular cell function in AKI?
Pigments such as myoglobin and crystals such as uric acid.
41
AKI Investigations
* History and physical findings
-Drugs, autoimmune, urinary obstruction etc
* Creatinine level, urine output
* Imaging: X-ray, USG, CT
42
AKI Management
* Fluid if pre-Renal AKI caused by hypovolemia
* Avoid any further insult to the kidneys such as
nephrotoxic drugs
* Limit the dietary ingestion of potassium and phosphorus
* Dialysis in patients with complications of AKI, such as
severe and nonresponsive hyperkalaemia and pulmonary
oedema.
* Correction of the metabolic abnormalities
* Treatment specific to the cause
43
What are risk factors to chronic kidney disease?
- Age
- race or ethnic group
- Genetic factors
- Hypertension
- Diabetes mellitus
- Metabolic Syndrome
44
How is chronic kidney disease (CKD) classified?
According to glomerular filtration rate (GFR).
45
What does glomerular filtration rate (GFR) measure?
The amount of blood filtered by the glomerulus per unit of time (mL/min), reflecting kidney function.
46
How long must impaired renal function persist to meet the definition of CKD?
47
What are the two main criteria for diagnosing CKD?
1. Impaired renal function for >3 months due to abnormal kidney structure or function.
2. GFR <60 mL/min/1.73m² for >3 months, with or without evidence of kidney damage.
48
Stage 1 of CKD
Mildest, few symptoms
* Kidney damage*
* Normal or relatively high GFR >90
49
Stage 2 of CKD
* Mild reduction in GFR 60-89
* Severe illness, poor life expectancy if untreated
* Established chronic kidney disease
50
Stage 3 CKD
* Moderate reduction in GFR 30-59
51
Stage 4 CKD
Severe reduction in GFR 15-29
52
Stage 5 CKD
Established kidney failure GFR <15
* or permanent renal replacement therapy (RRT)
53
What are the causes of CKD?
- Diabetes
- Hypertension
- Glomerulonephritis
- Pyelonephritis
- Unknown
54
CKD Management
* A naemia—treat with erythropoietin
* B ones (PO4 binders; active vit D)
* C ardiovascular: treat blood pressure
* D iet – low phosphate / sodium / protein
55
What is the medical term for kidney stones?
Nephrolithiasis (also known as renal calculi).
56
What are kidney stones composed of?
Crystal concretions typically formed in the kidney.
57
How common is nephrolithiasis worldwide?
It affects about 12% of the world’s population.
58
What is the most common condition affecting the urinary system?
Nephrolithiasis (kidney stones).
59
Kidney stones are associated with an increased risk of which chronic diseases?
Chronic kidney disease, end-stage renal failure, cardiovascular diseases, diabetes, and hypertension.
60
Risk Factors Kidney Stones
- Personal history of prior kidney stones
- Family history of kidney stones
- Increased enteric oxalate absorption
- Urinary tract infections
- Low fluid intake
- History of diabetes, obesity, gout and hypertension
61
What key urine change underlies the formation of kidney stones?
Supersaturation of solutes in urine.
62
Which solutes commonly supersaturate and precipitate in the urine to form stones?
Calcium, phosphorus, uric acid, oxalate, and cystine.
63
What is the process by which solutes precipitate and form kidney stones?
Nucleation and crystallization (crystal concretions).
64
Which two factors influence the transformation of urine from liquid to solid crystals?
Urine pH and the concentration of excess substances.
65
Calcium oxalate crystal
* Envelope or dumbbell-shaped
* A primary component of the majority of stones
* Typically occur in the setting of:
- Hypercaciuria
- Hyperoxaluria
- Hypermagnesuria
- Hypocitraturia
- Hypercysterinuria
66
Hypercalciuria
elevated levels of calcium
in the urine
67
Hyperoxaluria
elevated levels of oxalate
in the urine
68
Hypermagnesuria
elevated levels of
magnesium in the urine
69
Hypercystinuria
elevated levels of cystin
in the urine
70
Hypocitraturia
reduced levels of citrate in
the urine
71
Calcium phosphate crystal
Amorphous, wedge-shaped prisms in rosettes
72
Magnesium ammonium phosphate crystal
* Coffin lid shaped
* Also known as struvite stones
* Occurs in bacterial infection that produce urease (e.g Klebsiella pneumonia, Enterobacter, and Pseudomonas aeruginosa)
* The urease produces ammonia and CO2, which creates basic pH urine (>7).
73
Uric acid crystal
* Rhomboid shaped
* Typically idiopathic
* Occur in patients whose diets are high in protein, which acidifies urines pH (<7), allowing
for uric acid stone formation.
74
Cystine crystal
* Hexagon-shaped
* Caused by a genetic defect in the transport of the amino acid cystine, resulting in hypercystinuria.
75
Can nephrolithiasis present without symptoms?
Yes, it can be asymptomatic.
76
What type of pain occurs when a kidney stone descends the ureters?
Dull, colicky, sharp, and severe pain.
77
What causes the severe pain in ureteric kidney stones?
Peristalsis of the genitourinary tract smooth muscle against the stone.
78
Why is hematuria common in nephrolithiasis?
Injury to the genitourinary tract from the stone
79
What systemic symptoms may develop if a kidney stone becomes infected?
Fever and chills.
80
What may a physical exam reveal in a patient with nephrolithiasis?
Costovertebral tenderness.
81
Complications
* Abscess formation
* Sepsis
* Urinary fistula formation
* Ureteral scarring and stenosis
* Ureteral perforation
* Renal function loss due to long-standing obstruction
82
Investigations for Kidney Stones
Blood tests
- Serum creatinine
- Urea
Urinalysis:
- Urine electrolytes
- Urine pH
Imaging:
- A KUB X-ray
- CT of the abdomen and pelvis
- USG
83
Treatment of kidney stones
- Pain control
- Increase fluid intake
- Medications to aid stone passage and also reduces smooth stimulation
Systemic Pathology
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