Renal/urinary Conditions, Signs, Causes And Differentials Flashcards

1
Q

What are the three processes that cause renovascular disease?

A
  1. Renal artery stenosis (atherosclerosis causing narrowing of the arteries)
  2. Renal vein thrombosis (blockage)
  3. Renal atheroembolism (blockage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the renal conditions that cause secondary hypertension?

A

Primary renal disease (kidney parenchyma dysfunction):

  • Glomerulosclerosis,
  • Membranous nephropathy
  • Amyloidosis
  • Glomerulonephritis (glomerular inflammation)
  • Chronic kidney disease (decrease in GFR)
  • Polycystic kidney disease

Renovascular disease (blood supply is occluded or reduced)

  • Artery stenosis
  • Vein thrombosis
  • Atheroembolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which test result would point towards a renal cause of hypertension?

A

Increased creatinine

Due to either:
Renal parenchyma not filtering properly (expect progressive increase in creatinine)

Renal blood supply/drainage occlusion (expect an acute increase in creatinine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the differentials for proteinuria?

A
Benign orthostatic proteinuria
Physical exercise
Fever
Pregnancy
UTI
Abnormally high BP
Nephrotic syndrome (damage to the kidneys)
Nephritic syndrome (inflammation of the kidneys)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Through which pathophysiological process does CKD in diabetes progress?

A

Hypertension - high BP causes damage to the glomerulus via haemodynamic mechanisms.

This is why the single most important intervention for CKD is good blood pressure control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is diabetic nephropathy?

A

Disease of the kidney caused by diabetes

Since diabetes causes autonomic disfunction and damage to the blood vessels, this increases the likelihood of hypertension, as well as hyperglycaemia inducing the conversion of angiotensin 1 to 2, which also increases BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the four stages of diabetic nephropathy?

A

Basically: thicken at circumference, then thicken in centre, then nodules grow around centre, then nodules are diffuse and widespread

  1. Glomerular basement thickening (outer)
  2. Mesangial expansion (central)
  3. Nodular sclerosis (kimmelstiel-Wilson lesions; pink hyaline material in the capillary loops)
  4. More than 50% glomerulosclerosis; not nodular anymore but diffuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the pathological processes within the kidney that cause diabetic nephropathy?

A

In short: Hypertension and hyperglycaemia cause high pressure in the glomerulus, this damages the mesangium, and the nephron dies.

  1. Increased glomerular pressure due to:
    A - Hypertension in the body forces blood in to the glomerulus harder, increasing the glomerular pressure

B - Hyperglycaemia which causes the conversion of angiotensin 1 to angiotensin 2, activating the RAAS system

  1. The increased glomerular pressure, over time, causes barotrauma of the mesangium:
    A - cytokines release causing inflammation
    B - free radical formation
    C - mesangial expansion
    These processes cause podocyte foot processes to move apart, causing increase in fenestration size
  2. Nephron ischemia:
    A - Excess efferent arteriolar constriction reducing the supply to the vasa recta which supply the entire nephron (capsule to collecting duct)
    B - Free radicals and cytokines causing increased stress on the nephron
    These processes increase the rate of atrophy and destruction of the nephron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the progression of clinical findings in diabetic nephropathy?

A
  1. Increased GFR = early increased perfusion due to increased BP and RAAS activation
  2. Detectable proteinuria and microalbuminaemia = the start of barotrauma to the nephron due to dangerously high glomerular pressure
  3. Microhaematuria = the damage to the glomerulus is so bad, red blood cells (big) can get through the glomerulus and in to the tubule
  4. Kidney failure and decreased urine output = the nephrons are now starting to die and can’t filter anything
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is chronic kidney disease?

A

In short: Either structural abnormality/abnormal blood/urine results for >3 months or GFR <60 for 3 months, on TWO separate occasions 90 days apart.

A progressive, irreversible, chronic condition of damage to the kidney or reduced kidney function, defined by:
1. A)Evidence of damaged renal parenchyma as demonstrated by active urinary sediment (proteinuria or haematuria)

  1. B)and/or structural abnormality
  2. C)and/or evidence of decreased kidney function as demonstrated by a reduced GFR <60
  3. Plus CHRONICITY for >3 months (or it isn’t distinguished from AKI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of CKD?

A

Normally asymptomatic

Only in advanced disease do you acquire symptoms:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do the causes of CKD differ between old people and younger people?

A

Most people are elderly - CKD due to HTN/Macrovascular disease/DM

Young people - CKD more often due to glomerulonephritis and genetic causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is rapidly progressing renal failure?

A

Renal disease that progresses fast, over a matter of weeks or months.

Most often due to vasculitis, sarcoidosis or another systemic disease that targets the kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is end stage renal disease?

A

An individual who requires haemo replacement: dialysis or transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is azotaemia?

A

Azotaemia is elevation of nitrogenous metabolic waste in the blood due to failure of clearance by the kidneys.

Azotaemia = uraemia but asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is uraemia?

A

Uraemia is the clinical syndrome from failing kidneys and progressive azotaemia

Uraemia = azotaemia + symptoms/signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of CKD?

A

DM - most common
HTN - second most common
Glomerulonephritis- 3rd most common (a group of conditions, including autoimmune and infection)

Autoimmune disease 
Systemic sepsis
UTI
Renal stones
Urinary obstruction
Drug toxicity - NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the symptoms of uraemia?

A
Nausea
Vomiting
Weakness and fatigue 
Pruritis 
Neurological symptoms
Weight loss
Uraemic pericarditis

Uraemia is unlikely to occur in patients since by the time they get close to uraemia (kidney failure) they will be dialysed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why does metabolic acidosis occur in renal failure?

A

The kidneys reduce their production and reabsorption of bicarbonate - reduced buffering.

Increased protein catabolism occurs and this produces lots of organic acids - increased acidity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What kind of unusual infections do renal transplant patients have?

A

Since they are immunosuppressed in order to prevent rejection, infections like:

Cytomegalovirus colitis (long history of diarrhoea)
Pneumocystitis jirovecii pneumonia (long history of cough or crackles on chest)
Perforated diverticulitis
Cholecystitis
Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes pruritis in CKD?

A

Phosphate homeostasis is disrupted in CKD, this is due to decreased renal excretion.

Hyperphosphataemia results, which causes the pruritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is glomerular disease?

A

A term to describe a group of diseases that affect the glomeruli of the kidney (common cause of ESRD and CKD)

It involves:

  1. Inflammation - glomerulonephritis
  2. Damage to the functional mechanism of the glomeruli without inflammation - glomerulopathies

In practise the two of these pathological processes can overlap in a glomerular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are glomerular diseases distinguished?

A

They all have similar sets of signs and symptoms, so are called glomerular syndromes.

They can only be distinguished by biopsy and histopathological classification.

Classification:

  1. Glomerular syndrome (or not)
  2. Glomerular pathology type
  3. Primary, idiopathic or secondary cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is glomerular nephritis?

A

A group of diseases in which there is damage to the glomeruli, this can be due to many different causes; viruses, bacteria, autoimmune, drugs and others.

Most are due to immune-responses to causal agents. Not all types of glomerulonephritis present with nephritic syndrome.

Presentation can be nephrotic syndrome, nephritic syndrome (acute glomerulonephritis or rapidly progressive glomerulonephritis), CKD, just haematuria or just proteinuria

MOA: Activation of the innate and adaptive immune systems due to;

  1. Kidney=antigen - Reacting to a component of the glomeruli (acting as antigen)
  2. Antigen=filtered - Deposition/trapping of antigens in the glomeruli
  3. Antigen/antibody=filtered - Trapping of circulating immune complexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the causes of glomerular nephritis?

A

Bacteria: Group A streptococci
Viruses: Hepatitis B/C, HIV, malaria, leprocy, endocarditis, other
Respiratory and GI infections
Drugs: NSAIDs, cocaine, anabolic steroids, penicillamine, heroin
Metabolic disorders: DM, HTN, thyroiditis
Malignancy: lung and colorectal, melanoma, Hodgkin’s lymphoma

Lots of others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does glomerular nephritis present?

A

The presentation is variable:

  1. Just haematuria or proteinuria or both
  2. Reduced eGFR, and increased ACR - Chronic kidney disease
  3. Acute nephritic syndrome - Acute glomerulonephritis
  4. Rapidly progressive glomerulonephritis
  5. Nephrotic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is nephritic syndrome?

A

In short: immune complexes damaging the capillary endothelium allow RBCs, WBCs, AND proteins (less than nephrotic syndrome) through the glomerular membrane

Nephritic syndrome is a collection of signs and symptoms that indicate damage to capillaries and basement membrane of the glomeruli

  1. Haematuria
  2. Sub-nephrotic syndrome proteinuria
  3. Hypertension

MOA: Immune complexes deposit in the capillaries, these draw WBCs with them which cause an inflammatory response causing inflammation and breakdown of the capillary endothelium, these make big fenestrations, allowing blood, protein and WBCs through in to the urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the signs of nephritic syndrome?

A

All the signs of nephrotic syndrome: Loss of serum albumin, increased lipids, increased risk of PE/DVT due to loss of AT-3

Haematuria
Oliguria
HTN
Granular casts (white cells)

29
Q

What are the difference between nephritic and nephrotic syndrome?

A

Both affect the glomeruli of the kidney. (GBM = negative, albumin is negative)
(Endothelium = positive, RBCs are positive)

Nephrotic = High proteinuria, hypoalbuminaemia, hyperlipidaemia, oedema
MOA: Damage to loss of podocytes (small fenestrations and -ve)

Nephritic = lower proteinuria, haematuria, pyuria, inflammatory debris, HTN
MOA: Immune-mediated damage to the capillary endothelium (large fenstrations)

Note that most damage to the glomeruli will be immune-related, in both nephritic and nephrotic syndromes, the syndromes are only the presentation, not the aetiology.

30
Q

What is nephrotic syndrome?

A

In short: Podocyte loss and proteinuria
This is the process which often results during the process of chronic kidney disease, due to podocyte loss.

MOA: Podocytes die, their foot processes don’t interlock, and so they can’t prevent movement of midsize proteins from escaping the blood.

This result in loss of up to 3.5g of protein per day, which causes:

  1. Frothy urine - proteins in urine
  2. Oedema - albumin decline
  3. Increased serum lipids - liver compensation
  4. Hypercoagulable state - loss of antithrombin 3 protein, protein C and protein S
  5. Increased risk of PE and DVT - loss of anticoagulants
31
Q

What are the types of condition that cause nephrotic syndrome?

A

Nephrotic syndrome: High proteinuria, hypoalbuminaemia, hyperlipidaemia and oedema

  1. Minimal change - most common cause in young children
  2. Focal segmental glomerulonephritis (FSGS) - only some glomeruli affected, only parts of the glomerulus affected, commonest cause in adults
  3. Membranous glomerulonephritis -a second membrane forms over trapped immune deposits on the basement membrane forming irregular spikes
  4. Membranoproliferative glomerulonephritis - Same as 3 but the deposits are in basement membrane AND the mesangium

These all result in nephrotic syndrome but they are only distinguished by histopathology.

32
Q

What is minimal change disease?

A

A condition that presents as nephrotic syndrome.
A syndrome of heavy proteinuria, oedema, hypoalbuminaemia and hyperlipidaemia that most commonly affects children.

It is a nephrotic syndrome type, there are minimal changes to the kidney on histological analysis, hence “minimal change”.

33
Q

What is focal segmental glomerulosclerosis?

A

A condition that presents as nephrotic syndrome.
Most common cause of nephrotic syndrome in adults.
A chronic pathological process due to injury to the podocytes and causes a nephrotic syndrome (HTN, Oedema, hypoalbuminaemia and hyperlipidaemia).

MOA: Damage occurs to podocytes in a particular focal area of a glomerulus, the central cells (endothelial, mesangial) proliferate outwards in to this space, this segment has its capillary loops collapse, which then means the segment then undergoes sclerosis.

Some glomeruli are affected - focal
Only some podocytes on a glomerulus are affected but they cause sclerosis of the capillaries/mesangium behind them - segmental

34
Q

What is membranous glomerulonephritis?

A

A condition that presents as nephrotic syndrome.
A common cause of nephrotic syndrome in adults.
An immunologically mediated disease of the glomerular basement membrane.

MOA: Immune complexes deposit in the basement membrane (due to autoimmune, infection, drugs, malignancy, other), these then have a second membrane grow over them, this damages podocytes somehow.

35
Q

What are the broad categories of causes of nephrotic syndrome?

A
  1. Primary or idiopathic
  2. Secondary:
    Autoimmune, infection, drugs, heavy metals, tumours, diabetic nephropathy (kimmelstiel-Wilson lesions)
36
Q

What are the conditions that can cause nephritic syndrome?

A

Nephritic syndrome: Haematuria, sub-nephrotic range proteinuria and HTN

IgA nephropathy

Postinfectious glomerulonephritis (-post streptococcal)

Rapidly progressive glomerulonephritis:

  • vasculitis
  • anti glomerular basement membrane glomerulonephritis
  • Lupus
  • Henoch–Schönlein purpura
37
Q

What is poststreptococcal glomerulonephritis?

A

A condition that presents as nephritic syndrome, a type of acute glomerulonephritis.

Group A beta-haemolytic streptococci carry enzymes that lyse RBCs, when in the body they induce a type 3 hypersensitivity reaction. Antigens from the bacteria become complexed to antibodies.

Occurs 1-3 weeks after infection.
Can progress to rapidly progressive glomerulonephritis.

MOA: The immune complexes become trapped in glomerulus, which causes compliment activation and damage to the basement membrane.
This allows RBCs through, and protein loss, causing nephritic syndrome.

Causes: Impetigo and pharyngitis, most often affects children

38
Q

What is IgA nephropathy?

A

A condition that presents as nephritic syndrome, a cause of rapidly progressive glomerulonephritis.
IgA nephropathy is the most common cause of glomerular nephritis.

Occurs 1-3 days after infection.
Can progress to rapidly progressive glomerulonephritis.

MOA: Most commonly occurs a few days after an upper respiratory tract infection, can also be GI or urinary infection. Again,like PSGN, immune complexes form (antigen+antibody) and deposit in the glomeruli causing nephritic syndrome.

39
Q

What is rapidly progressive glomerulonephritis (crescenteric glomerulonephritis)?

A

A condition that presents as nephritic syndrome. Similar to the pathophysiology in membranous and membranoproliferative glomerulonephritis (nephrotic syndrome).

MOA: Antibodies or immune complexes cause Inflammation of the kidney glomeruli.

  1. Anti-glomerular basement membrane (Anti-GBM)
    - Against the basement membrane
  2. Immune-complexes
    - Against blood borne viral/bacterial/physiological antigens
  3. Anti-neutrophilic cytoplasmic antibody (ANCA)
    - Against neutrophils

This induces proliferation of cells in the bowmans space, where they thicken the parietal surface of the bowmans capsule, which causes nephritic syndrome and rapid renal failure (weeks to months).

40
Q

What is type 1 rapidly progressive glomerulonephritis?

A

A condition that presents as nephritic syndrome.
Anti-glomerular basement membrane antibodies attacking the basement membrane.

Associated with good pastures syndrome and pulmonary haemorrhages.

Shows crescent shaped glomeruli on histopathology investigation, just like all the types of rapidly progressive glomerulonephritis.

41
Q

What are the causes of type 2 rapidly progressive glomerulonephritis?

A

A condition that presents as nephritic syndrome.
This is an immune-complex mediated disease, so the causes are:
1.Post-streptococcal glomerulonephritis (PSGN)
2. Lupus
3. IgA nephropathy
4. Henoch–Schönlein purpura

All either produce antigens to complex with, or complex to normal antigens found in the body (e.g. kidney receptors or other)

Shows crescent shaped glomeruli on histopathology investigation, just like all the types of rapidly progressive glomerulonephritis.

42
Q

What are the causes of type 3 rapidly progressive glomerulonephritis?

A

A condition that presents as nephritic syndrome.
Type 3 = not AntiGBM and not immune complex

They are caused by anti-neutrophilic cytoplasmic antibodies.

Types:
1. cANCA = cytoplasmic antibodies
Cause - wegners granulomatosis

  1. pANCA = perinuclear antibodies
    Causes - microscopic polyangiitis and churg-Strauss syndrome

Shows crescent shaped glomeruli on histopathology investigation, just like all the types of rapidly progressive glomerulonephritis.

43
Q

What is granulomatous inflammation?

A

This is a process by which immune cells try to wall off foreign substances.

44
Q

What are the autosomal dominant causes of cystic renal disease?

A

Autosomal dominant:
1. Autosomal dominant polycystic kidney disease

  1. Tuberous sclerosis
  2. Von Hippel Lindau syndrome
  3. Medullary cystic disease
45
Q

What are the autosomal recessive causes of cystic renal disease?

A

Autosomal recessive:
Autosomal recessive polycystic kidney disease
Juvenile onset nephronphthisis

46
Q

What are the X-linked causes of cystic renal disease?

A
X-linked:
Orofacial digital syndrome
Trisomy 13 Patau
Trisomy 18 Edwards
Trisomy 21 Down
47
Q

What are the types of non-genetic acquired cysts?

A

Acquired cysts:
Simple cysts
Acquired renal cystic disease
Hypokalemia related cysts

MOA: Acquired cysts often are acquired due to age and renal failure.

48
Q

What are the types of non-genetic developmental cysts?

A

Developmental:
Medullary sponge kidney
Multicystic dysplasic kidneys
Pyelocalyceal cysts

49
Q

Which type of renal cysts become more common with age?

A

Simple cysts become more common with increasing age

Over the age of 30 simple cysts can occur.
People over the age of 50 most often have at least one simple cyst.

Characteristics:
Unilocular
Located in the cortex
No kidney enlargement

50
Q

Which renal cystic disease most commonly causes renal failure?

A

Autosomal dominant polycystic kidney disease is the most common cystic disease that causes renal failure.

ADPKD causes 10% of dialysis patients.

51
Q

How can you distinguish autosomal dominant and recessive polycystic kidney disease?

A
  1. Inheritance pattern: vertical transmission in ADPKD, and not seen in every generation in ARPKD
  2. Early onset in infancy in ARPKD, normally presents in childhood
  3. ARPKD causes congenital hepatic fibrosis; liver disease, whereas ADPKD dose cause cysts in liver/pancreas/spleen, they are often asymptomatic
52
Q

What are the possible signs of renal cysts?

A
  1. Asymptomatic
  2. Haematuria
  3. Abdominal pain
53
Q

What is autosomal dominant polycystic kidney disease?

A

ADPKD is the commonest genetic renal disease, it is the development of fluid-filled cysts throughout the medulla and cortex causing organ enlargement and chronic kidney disease.

It occurs due to a defect in either:
A) PKD1 on chromosome 16 (85%)
B) PKD2 on chromosome 4 (15-20%)

These cause dysfunction in product protein polycystic 1 or 2 respectively, which causes aberrant cell signalling, disorganised cell growth and fluid secretion.

Extrarenal presentations:

  1. Berry aneurysms (- an aneurysm that looks like a berry and typically occurs in the circle of Willis where the circle bifurcates)
  2. Cysts in liver/pancreas/spleen
  3. Mitral valve prolapse
54
Q

What are the clinical features (symptoms, signs) of ADPKD?

A
Symptoms:
Young
Flank/abdominal pain
Renal colic
Gross haematuria

Cystitis recurrence symptoms:
Dysuria
Urgency
Suprapubic pain

Early features:
Polyuria/nocturia
HTN

Fever/abdominal pain (- infection of cyst)
Loin/abdominal pain
Palpable renal or hepatic mass
Proteinuria
Frank haemturia (- often temporary)

Late features:
End stage renal failure (uraemia, HTN, low eGFR, fatigue, muscle pains, etc)

Extrarenal manifestations:

  1. Polycystic liver disease (abdominal pain, early satiety, gastrooesophageal reflux, Dyspnoea, obstruction of biliary tree, cystic infection/inflammation)
  2. Left ventricular hypertrophy
  3. Mitral valve prolapse
  4. Pericardial effusion
  5. Berry aneurysm
  6. AAA
  7. Abdominal hernias
  8. Diverticular disease
55
Q

What is Von Hippel-Lindau disease (VHL)?

A

An autosomal dominant disease, presenting with an array of tumours, affecting the CNS, retina and kidneys.

The gene is on chromosome 3, codes a protein that acts as a tumour suppressor gene (among other things).

Presentation: In 20-30’s (delayed expressivity)

Renal manifestations:

  1. Cortical renal cysts (75% have these)
  2. Bilateral, multicentric renal cell carcinoma (20-45%, can be unilateral, can be monocentric; only one primary tumour)
  3. Renal cell adenoma
  4. Renal hemangioma (collection of small blood vessels)
  5. Renal haemangioblastoma (normally only in CNS)
    - All of these can cause bleeding-
56
Q

What is acute kidney injury?

A

A syndrome characterised by rapid reduction in renal function due to various causes, signs are those caused by reduced excretion. AKA acute renal failure

MOA: Most commonly due to reduced blood flow to the kidney, so anything that can do that. (Can also b3 caused by acute tubular necrosis)

Signs - Most commonly nondescript (like CKD), may include tiredness, Dyspnoea, nausea or confusion

Staging is based on serum creatinine and urine output: stages 1,2 and 3
Where stage 1 is increased SCr by 1.5-1.9 times reference and less than 0.5ml/kg/hr urine output

Stage 3 is incr SCr by 3 times reference and less than 0.3ml/kg/hr urine output

Causes are pre-renal, renal and post-renal.
Common causes in the elderly:
Prerenal = Sepsis, diarrhoea, diuretic (all reduce flow)
-> most common cause 85%!
Renal = ACEI/ARBs and NSAIDs
Postrenal = Renal stones, prostate cancer, BPH or bladder malignancy (Obstructions)

57
Q

What are iatrogenic causes of AKI?

A

Drugs: NSAIDs, ACEI, ARBs, gentamicin
All cause Renal AKI

Contrast for CT, also renal!

Surgery causing loss of blood

58
Q

What are conditions that can be a prerenal cause of AKI?

A

Severe HF
Sepsis
Hypotension
Shock
Primary liver disease (causes hepatorenal syndrome: meaning renal vasoconstriction occurs )
Intraabdominal hypertension
Compartment syndrome (when oedema or haemorrhage occurs, it cuts off circulation to that area, creating a “compartment”)

59
Q

What is acute tubular necrosis?

A

The end product of renal ischemia and toxicity, it is the death and loss of renal parenchyma (doesn’t have to accompany loss of renal function, but can, in which case it can cause AKI)

Causes sloughing of renal tubular epithelium and leukocyte infiltration

Stages: - in short = Poor function due to ischemia or toxicity, then kidney goes too far and overcompensates (decreases its reuptake)

  1. Oligouric; decreased urine output, high creatinine and vulnerable to fluid/electrolyte overload
  2. Maintenance; all of the above improve
  3. Polyuric; urine output is very high (causing hypovolaemia and electrolyte loss), electrolytes are lost and creatinine falls fast

(MOA: Aquaporin channels recover last, so no water reuptake occurs, like having diabetes insipidus or adrenal insufficiency - hypoaldosteronism)

60
Q

What is the most common renal cancer?

A

Renal cell carcinoma

Causes: haematuria, flank pain and growth of a mass

Occurs in 40-60 age bracket

Second most common is transitional cell carcinoma
Causes: Haematuria, flank pain and dysuria

61
Q

What are the main benign types of renal cancer?

A

Angiomyolipoma and oncocytoma

62
Q

What is papillary necrosis?

A

The necrosis and shedding of renal medullary papillae (where the pyramids empty in to the minor calyx) due to infarction

Presents with renal colic, haematuria and infection (exactly like a renal stone)

63
Q

What is ADPKD?

A

Autosomal dominant polycystic kidney disease, the commonest renal genetic disease

Cysts form in kidney, liver, pancreas, spleen, or brain
Onset: Any time in life

64
Q

What is Von Hippel Lindau disease?

A

A

65
Q

What are the signs of a lower urinary tract infection?

A

Frequency
Urgency
Dysuria

66
Q

What are the signs of pyelonephritis?

A

Loin pain spreading to the back, unilateral
Pyrexia
Systemic unwellness

67
Q

What are the signs of bladder cancer?

A

Haematuria- frank or microscopic
Irritative urinary symptoms
Complicated UTIs

68
Q

Which stages of bladder cancer invade the muscle wall?

A

Stages T2 onwards

T4 has passed in to adjacent organs (prostate, uterus)

Note: stage pTa and stage cis are confined to the epithelium

69
Q

What are the histological signs of bladder cancer?

A

Hyperdense nuclei
Overlapping nuclei
Cells are less distinct from each other
Nuclear polymorphism occurs