Lecture 7: Haematuria and Proteinuria Flashcards by sita clark

Clinical Presentation and Clinical Problem associated with generalised Parenchymal kidney Disease

Clinical presentation:

Clinical Problem:

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Clinical Presentation and Clinical Problem associated with generalised Collecting System Abnormality kidney Disease

Clinical presentation:

Clinical Problem:

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Clinical Presentation and Clinical Problem associated with generalised Focal leson assoc. kidney Disease

Clinical presentation: Haematuria, backache

Clinical Problem:

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Extremes of changed glomerular function

Blocked Leaky
Siv b/w
- may or may not ahve lead to a change in GFR

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Blocked (glomerular) filter

Blocked filter = reduced GFR

acute Kidney injury
chronic kidney disease

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Proteinuria

Kidney handle 150L filtrate/day
Normal humans <150mg/24hrs. 
Barriers to urinary protein:
1. Glomeruli - filters protein
2. Tubules - reabsorbs and filters

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Affect of damaged glomerulus + High Blood Pressure

Increased leaked protein –> Proteinuria

2. High Blood pressure –> Increased damage to glomerulus –> worsening of situation/leakiness

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Leaky filter

Leaking of blood or protein through glomerulus
Kidney function may be normal
Creatinine goes through glomerular filter, but not proteins
Note: every glomerulus will leak a little bit of protein into our urine

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Proteinuria

Mainly albumin
Other proteins in small amounts
Measurements:
1. 24 hour urine --> annoying
2. Albumin: creatinine 
3. Protein : creatinine
Note: 2x ratios are good surrogates replacing 24hour urine collection

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Microalbuminuria

(albumin:creatinine ratio)
30-300 albumin/24 hours
ACR: x < 2.5 - y - 25 < z (mg/mmol/24 hours)
x= normal y= MA z= proteinuria
Causes: Diabetes Mellitus, Fever, Exercise, HF, Poor Glycemic control

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Diabetes Mellitus relatively increases risk of..

Heat disease
Eye disease
Kidney fialure

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Nephrotic Sydrome

Signs of nephosis: Proteinuria, Hypoalbuminaemia, odema
>3.5 g/day urinary protein
- eat protein but pee out more than they can eat
Symptoms:
1. Frothy urine
2. Reduced metabolism (VLDL - LDL) –> Increased Tryglycerides
3. Blood clots –> Pulmonary embolism
4. Normal or impaired Renal function/GFR
5. Low plasma oncotic pressure –> Increased lipoprotein production by liver –> increased cholesterol production –> hypercholesterolemia –> increase risk of vascular disease

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Mechanism for Oedma

Increased albumin excretion –> Food and liver cant keep up with making enough albumin –> Low levels of protein in blood –> Reduced vascular oncotic pressure –> Increased egression of fluid into interstitial space (in an attempt to balance colloid oncotic and hydrostatic pressure b/w BV and tissues

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Reason for Nephrotic Syndrome Oedema

Decreased protein and increased water in vasculature –> Decreased vascular oncotic pressure and increased hydrostatic pressure –> trying to balance equilibrium by pushing water into Extracellular spaces (cannot move proteins through filter) –> odema

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Starling’s Equation

Flux = capillary permeability (intravascular hydrostatic pressure - interstitial hydrostatic pressure) - (intravascular oncotic pressure - interstitial oncotic pressure)
Capillary hydrostatic P: pushes fluid out of vessel if high
Capillary oncotic pressure : pulls fluid into vessel if high. Derived from plasma proteins

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Glomerular injury –> Odema

Glomerular injury –> protein leakage into interstitial space (bowmans space) –> Decrease in Plasma volume and Cardiac output –> Arterial hypervoluemia –> stimulation of RAAS –> Sodium and H2O retention –> Expansion of sodium space –> Odema

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Relationship b/w Lipids and cholesterol and Nephrotic syndrome

Reduced metabolism (VLDL - LDL) –> Increased Tryglycerides
Low plasma oncotic pressure –> Increased lipoprotein production by liver –> increased cholesterol production –> hypercholesterolemia –> increase risk of vascular disease

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Thrombolism

Risk factor of Nephrotic Syndrome
Pathophysiology not well understood (Risk 10%)
Nephrotic syndrome –> increase risk of DVT and pulmonary emboli –> clot in leg/femoral artery –> swollen, red and painful –> risk of embolus –> travels to lungs –> right heart failure –> death

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Infection

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Reduced antibody production and decreased complement pathway

Increased bacterial infection and chicken pox in children

Protein malnutrition

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Risk in nephrotic syndrome/ Microalbuminuria / proteinuria

Protein malnutrition –> wasted, lost weight and unwell

Diabetic Neuropathy

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Increased lumps of matrix int he glomerulus = leakage of protein into the urine
Type I Hyperglycaemia –> high serum glucose –> increased GFR/hyperfiltration due to high hydrostatic pressure
- IF have good glycaemic and BP control can have normal GFR w/o protein leaking
BUT Low GFR –> leak protein into urine Preceding decline due to kidney damage/Nephrotic syndrome
** graph

CKD

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Often due to glomerular disease
Other major cause is diabetes (would just have protein in blood)
Blood or protein in urine (only protein in DM)
CKFailure
Main treatment is controlling BP (ACE inhibitors)

AKI

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Pre renal, renal, post renal
Rena; = intrinsic (specific to kidneys) AKI –> Acute Tubular necrosis (from prerenal/drugs) –> Acute glomerulonephritis –> may have proteinuria

Acute Tubular Necrosis

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Due to:
1. Prerenal inadequate treatment
2. Drugs/toxins
No blood or protein in urine
Just decreased GFR (renal function) due to blocked filter

Acute Glomerulonephritis

= Rapidly progressive glomerulonephritis = Acute Renal Failre Leaky glomeruli AND Blocked (fluid overload): Blood +/- protein May have nephritic syndrome

Nephritic Syndrome

Occurs in Acute/Rapidly progressive glomerulonephritis/ Acute Renal failure Leaky + Increased GFR Fluid overload as only able to excrete a limited amount of fluid per day --> peripheral and pulmonary oedema Symptoms/Signs: 1. Unwell 2. Oliguric 3. Hypertensive --> 4. Volume overload --> pulmonary/peripheral oedema 5. Signs of other Multi-System disease: a) haemoptysis b) rash c) arthritis d) fever 6. MSU (blood/protein) --> Red Clast cells

Diagnosis of Nephritis syndrome/ Rapidly progressive/Acute Glomerulonephritis

1. Kidney Biopsy 2. Blood in urine (sometime protein) - -> Red Clast cells = Broken down RBC all clumped together

Nephrotic syndrome vs nephritic syndrome

NephrOtic syndrome: Oedema, Proteinuria, Hypoalbuminuria, Renal Function/GFR can be normal or impaired Nephritic syndrome: ARI, Hypertension --> Fluid overload --> Pulmonary and peripheral oedema, RBC in urine --> Clast cells (damaged RBC cell clumps) in blood sample

Haematuria

Micro - in most people Macro - clots if severe Note: If blood in urine --> NEED TO EXCLUDE CANCER - high chance is catch early

Origins of Haematuria

Bleeding from somewhere in urinary tract: 1. Glomerular (e.g. glomerulonephritis) 2. Collecting System (tumour/stone) 3. Focal lesion (ureters/stone/bladder/urethra)

Glomerular Haematuria type of Haematuria

Proteinuria + Haematuria --> increased likelihood of glomerular haematuria - often microscopic - often (but not always) assoc. with proteinuria

Haematuria from Collecting System

Could be due to tumour/kidney stone (radiologically diagnosed) Usually macroscopic No/little protein 1. Loin-Groin pain= very severe and collical (due to contraction) 2. Hematuria (clots) 3. Vomiting/Nausea

Causes of Haematuria

1. Malignant 2. Inflammatory 3. Infectious 4. Kidney Stone

Bilateral kidney sone blockage

Anuria --> Post renal Acute Injury

Hydronephrosis radiological appearance

Blockage of urethra = Black hole CT see white stone Treatment: 1. Pass stone spontaneously. 2. Require surgery/Lazering of the stones (Lythotrixy)

Focal lesions as cause of Haematuria

Focal lesion : tumour (tumour anywhere in the urinary tract can cause bleeding) Macro/microscopic Often asymptomatic (due to late diagnosis/ can be large and have been there for a long time) Back-ache (when really bad, as late symptomatic presentation) Mass (extraordinarily bad if can see mass. Note: is now quite uncommon due to screening)

Types of Focal lesions causing haematuria

Renal cell carcinoma in corex Transitional cell carcinoma in urothelium bladder cancer prostate cancers --> blood enters uring due to erosion

Radiology for Focal lesions

CT scan: can diagnose renal cell carcinoma

Renal cell carcinoma

90% of renal cancer (primarily from renal cells. Not metastatic or transitional) 2 Male: 1 Female Peak 6th decade Aetiology: 1. Smoking 2. Genetic: von hippel-Lindau disease (sporadic cases have 3p abnormalities)

Renal cell carcinoma Macroscopically

well circumscribed mass Mottled red, yellow and brown Part cystic May invade renal vwin

Clinical picture of Renal cell carcinoma

``` Symptoms occur late Haematuria - may be clots Flank pain (if extremely big) Palpable abdominal mass Ectopic hormone production Risk of Spreading/MEts ```

Ectopic hormone production due to Renal Cell Carcinoma

``` Polycythemia (EPO) Hypertension (renin) Hypercalcemia Cushing Syndrome (cortisol) Feminisation or masculinisation ```

Renal cell carcinoma risk of Metastatic spread

Local spread not common Mainly blood-born metastases: Lungs, bones, liver, adrenals, brain Regional lymph nodes Survival: overall ~ 40% 5 years ( Low survival tumour - often because late diagnosis)

Haematuria summary

can come from anywhere, need to make sure isn't kidney stone or cancer - Structural problem - Glomerular: may have proteinuria or renal failure, hypertension, usually microscopic - Collecting system: stones, infection, MBU, radiology - Focal lesion: tumour, radiology

Proteinuria/Haematuria summary

Blood and protein in urine abnormal Protein: usually glomerular --> leaky glomerulus. Can have renal impairment (blocked filter) Treatment: 1. Find cause. 2. Reduce pressure Haematuria: can be glomerular. Need to exclude malignancy, stone, infection

Lecture 7: Haematuria and Proteinuria Flashcards

(45 cards)