Lecture 7: Haematuria and Proteinuria Flashcards
Clinical Presentation and Clinical Problem associated with generalised Parenchymal kidney Disease
Clinical presentation:
Clinical Problem:
Clinical Presentation and Clinical Problem associated with generalised Collecting System Abnormality kidney Disease
Clinical presentation:
Clinical Problem:
Clinical Presentation and Clinical Problem associated with generalised Focal leson assoc. kidney Disease
Clinical presentation: Haematuria, backache
Clinical Problem:
Extremes of changed glomerular function
Blocked Leaky
Siv b/w
- may or may not ahve lead to a change in GFR
Blocked (glomerular) filter
Blocked filter = reduced GFR
- acute Kidney injury
- chronic kidney disease
Proteinuria
Kidney handle 150L filtrate/day Normal humans <150mg/24hrs. Barriers to urinary protein: 1. Glomeruli - filters protein 2. Tubules - reabsorbs and filters
Affect of damaged glomerulus + High Blood Pressure
- Increased leaked protein –> Proteinuria
2. High Blood pressure –> Increased damage to glomerulus –> worsening of situation/leakiness
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
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
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
Diabetes Mellitus relatively increases risk of..
Heat disease
Eye disease
Kidney fialure
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
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
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
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
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
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
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
Infection
Reduced antibody production and decreased complement pathway
Increased bacterial infection and chicken pox in children
Protein malnutrition
Risk in nephrotic syndrome/ Microalbuminuria / proteinuria
Protein malnutrition –> wasted, lost weight and unwell
Diabetic Neuropathy
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
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
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
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
- Kidney Biopsy
- 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:
- Glomerular (e.g. glomerulonephritis)
- Collecting System (tumour/stone)
- 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
- Malignant
- Inflammatory
- Infectious
- 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
