Renal conditions Flashcards
Renal Colic - Description
Renal stones (calculi) made of crystal aggregates form in collecting ducts and then deposited anywhere from renal pelvis to urethra
Renal Colic - Epidemiology
- More males
- 10% lifetime risk
- More in the Middle East
Renal Colic - Pathology
- Solutes in urine become too concentrated → supersaturated → solvent precipitates → crystals form
- Occurs when there is an increase in solute or a decrease in solvent (dehydration)
- Crystals make stones which cause obstruction → hydronephrosis (obstruction and dilation of renal pelvis → lasting kidney damage)
- Stones are made of: calcium oxalate (most common, in acidic urine), calcium phosphate (in alkali urine), calcium carbonate, uric acid, crystine, drug precipitants
- Stones are most commonly found in pelviureteric junction (most common), pelvic brim, vesicoureteric junction
Renal Colic - Types
- Upper urinary tract - renal stones, ureteric stones
- Lower urinary tract - bladder stones, prostatic stones, urethral stones
Renal Colic - Causes (7)
- Anatomical - congenital (horseshoe, duplex, pelviureteric junction obstruction, spina bifida) and acquired (obstruction, trauma, reflux)
- Urinary - dehydration, too much solutes
- Infection - UTIs with organisms that produce urease (Proteus, Klebsiella, Pseudomonas) produce specific types of stones called staghorn calculus
- Hypercalciuria - increased urinary calcium excretion (caused by hyperparathyroidism - most common, hypercalcaemia, eating too much calcium, prolonged immobilisation - bone reabsorption)
- Hyperoxaluria - increased oxalate means more clacium oxalate (eating too much oxalate, malabsorption, autosomal recessive enzyme deficiency)
- Uric Acid Stones - patients with ileostomies as they loose more bicarbonate so have acid urine so uric acid is more soluble
- Cystine stones - caused by an autosomal recessive condition, cystinuria
Renal Colic - Prevention (6)
- Reduce dietary salt / sodium
- Normal dairy intake
- Healthy protein intake (50-100g/day)
- Lose weight
- Active lifestyle
- Stop smoking
Renal Colic - Risk Factors (9)
- Anatomical abnormalities
- Hypercalciuria
- Hypercalcaemia
- Hyperparathyroidism
- Family history
- Hypertension
- Gout
- Immobilisation
- Dehydration
Renal Colic - Differential Diagnosis (9)
- Ruptured AAA
- Diverticulitis
- Appendicitis
- Pylonephritis
- Acute pancreatitis
- Ectopic pregnancy
- Ovarian cyst
- Ovarian torsion
- Testicular torsion
Renal Colic - Symptoms (6)
- Asymptomatic
- Loin pain, rapid onset, unable to get comfy, radiates to groin, N&V
- UTI symptoms - dysuria (painful urinating), strangury (burining urinating), urgency, frequency
- Shivering
- Recurrent UTIs
- Bladder distension
Renal Colic - Investigations (6)
- History - excess Vit D consumption leads to hypercalcaemia, excess rhubarb or tea leads to high oxalate
- X-Ray KUB (kidney, urethre, bladder) - first line
- Non-contrast CT KUB - gold standard
- Ultrasound - sensitive for hydronephrosis, good for pregnant or youth
- Urine dipstick - blood traces
- Bloods - FBC, U&E, Calcium, Uric acid, Creatinine
Renal Colic - Treatment (9)
- Ureteric stones
- Analgesia - diclofenac IV 75mg
- Anti-emetics - metoclopramide
- Allow 2 weeks for it to pass
- Drainage if septic
- ESWL (Extracorpeal Shock Wave Lithotripsy) - non invasive procedure breaks down stones, use if <1cm
- Kidney stones
- Analgesia - Diclofenac
- Anti-emetics - Metoclopramide
- ESWL - for stones 1-2cm
- Surgical - uteroscopy, percutaneous nephrolithotomy, nephrectomy
Renal Colic - Complications (3)
- Small stones migrate to ureter
- Large stones occlude calyces or uteric pelvic junction
- Chronic damage especially if it gets infected
AKI - Description
Abrupt deterioration (hours-days) in renal function (raised serum urea and creatinine) due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis. Usually reversible
AKI - Criteria for Diagnosis
- Creatinine increased >26 micromol/L in 48 hours
- Creatinine increased >50%
- Urine output <o.5ml/kg/hr for more than 6 hours
AKI - Epidemiology
- Associated with diarrhoea, haematuria, haemoptysis, hypotension, urine retention
- Common in elderly
- 25% with sepsis and 50% with septic shock have AKI
AKI - Causes
- Pre-renal - reduced blood flow to kidney leading to reduced GFR
- Shock, hypovolaemia, hypotension, Renal artery thrombosis, sepsis, renal hypoperfusion
- Renal - kidney can’t filter blood properly, cells damaged so reabsorption and secretion impaired
- Acute tubular necrosis, Nephrotoxins, Glomerulonephritis, Acute interstitial nephritis, Infection, Vasculitis, Malignant hypertension, Autoimmune disease
- Post-renal - blockage of kidney reducing outflow
- BPH, Kidney stones, Cancer, Blood clot
AKI - Risk Factors (8)
- > 75
- DM
- HF
- Sepsis
- PVD
- Family history
- Drugs
- Dehydration
AKI - Symptoms (11)
- Asymptomatic in early stages
- Oliguria (decreased urine output)
- Anuria (no urine output)
- Ddehydration
- N&V
- Tremor, weakness, fatigue, confusion
- Breathlessness (anaemia and pulmonary oedema from volume overload)
- Tachycardia
- Peripheral oedema (from hypertension)
- Poor tissue turgor
- Postural hypotension (dehydration)
AKI - Investigations (5)
- Urine dipstick - glomerulonephritis suggested by haematuria and proteinuria
- Bloods - Anaemia and high ESR suggest myeloma or vasculitis
- Renal ultrasound - shows obstruction, small kidney indicates CKD
- Monitor urine output
- KUB XR and non-contrast CT
AKI - Complication
Hyperkalaemia - when kidneys fail they go into cardiac arrest
AKI - Treatment (4)
- Treat underlying cause - pre-renal (fluids, antibiotics), post-renal (catheteris, cystoscopy)
- Stop nephrotoxic drugs - NSAIDs (aspirin, diclofenac, ibuprofen), ACEi (Ramipril), Gentamicin, Amphotericin
- Treat complications - hyperkalaemia, pulmonary oedema, uraemia, acidaemia
- Dialysis
CKD - Definition
Long standing, usually progressive abnormality of the kidney or a reduction of GFR to <60ml/min/1.73m2 for >3 months
CKD - Epidemiology
- 6-11% incidence
- Risk increases with age
- More females
- Highest mortality from cardiac complications
CKD - Classification/staging
- Stage 1: >90ml/min - Normal GFR with evidence of renal damage
- Stage 2: 60-89 - Slight decrease GFR with evidence of renal damage
- Stage 3A: 45-59 - Moderate GFR decrease with or without evidence of renal damage
- Stage 3B: 30-44 - Moderate GFR decrease with or without evidence of renal damage
- Stage 4: 15-29 - Severe GFR decrease with or without evidence of renal damage
- Stage 5: <15 - Established renal failure
CKD - Pathology
- Progression of end-stage kidney disease (ESRF) with varying speed of decline
- Many nephrons are failed so burden of filtration goes to functioning nephrons which experience hyperfiltration (increased flow per nephron as blood flow remains the same) → glomerular hypertrophy and reduced arteriolar resistance
- Stress means increased failure of functioning nephrons and cycle continues
CKD - Pathology of bone disease
Increased renal phosphate and reduced 1,25-dihydroxyvitamin D → reduced serum calcium → compensatory increase PTH → skeletal decalcification
CKD - Pathology of Anaemia
reduced erythropoietin production → less RBCs → anaemia. reduced production and excretion of hepcidin builds up and inhibits iron absorption → anaemia
CKD - Pathology of Hyperkalaemia
less potassium excretion → build up in blood
CKD - Pathology of CVD
decreased filtration → renin release → increase BP → cardiomyopathy, pericarditis (uraemia), bleeding (urea stops platelet binding)
CKD - Causes (7)
- Hypertension - walls thicken to withstand pressure → narrow lumen → less blood and O2 to kidney → ischaemic injury. Immune cells release TGF-B1 in damaged glomerulus → mesangial cells regress to immature mesangioblast and secrete extracellular matrix → glomerulosclerosis
- DM - Excess glucose sticks to proteins making efferent arterioles stiff and narrow → obstruction for blood leaving glomerulus → hyperfiltration → supportive mesagnial cells secrete structural matrix → increased size of glomerulus → glomerulosclerosis
- Glomerular disease - Nephrotic syndrome damages glomerular capillary call and decreases tubular protein reabsorption → renal tubular cell damage → inflammation → fibrosis of proximal tubular cells
- PKD
- SLE (Systemic Lupus Erythematosus
- Obstructive uropathy
- Nephrotoxic drugs
CKD - Risk Factors (9)
- DM
- Hypertension
- Age
- Female
- CVD, IHD, PVD
- SLE
- Family history
- UTIs
- BPH
CKD - Symptoms (11)
- Asymptomatic in early stages
- Urinary - oliguria, haematuria, proteinuria, nocturia, polyuria
- Non-specific - N&V, anorexia, itching, hiccups, lethargy, tremors, convulsions
- Bone disease - osteomalacia, osteoporosis, osteosclerosis
- Anaemia - pallor, lethargy, exertional breathlessness, bruising
- Hyperkalaemia - cardiac arrhythmias/arrest, weakness/paralysis, metabolic acidosis
- CVD - uraemic pericarditis, hypertension, PVD, HF
- Neurological - confusion, coma, fits
- Volume overload - pulmonary oedema, dyspnoea, ankle oedema
- Sexual dysfunction
- Increased skin pigmentation (yellow)
CKD - Investigations (2)
- Ultrasound - bilaterally small kidneys, excludes obstruction
- FBC - anaemia, raised creatinine, phosphate,PTH, K+, renin and urea, decreased Ca2+
CKD - Treatment (7)
- Treat underlying cause
- Manage BP (ABCD) - ACEi, Beta Blocker, Calcium channel blocker, Diuretic
- Statins - if GFR <60
- Lifestyle changes
- Stop nephrotoxic drugs
- Dialysis
- Transplant
CKD - Complications (8)
- Hyperkalaemia
- Osteoporosis - GFR <30 (give Bisphosphonates)
- Vit D deficiency (give Cholecalciferol)
- Anaemia
- Metabolic acidosis
- Pruritis
- Pericarditis
- Hypertension
ADPKD - Description
Multiple cysts develop gradually resulting in renal enlargement, kidney tissue destruction and gradual renal failure
ADPKD - Epidemiology
- Most common inherited kidney disease
- Presents 20-30
- More male than female
- Homozygous babies won’t survive
ADPKD - Causes (2)
- Mutation in PKD1 gene (85%) on chromosome 16 - more severe, earlier onset
- Mutation in PKD2 (15%) on chromosome 4 - less severe, later onset
ADPKD - Risk Factors (3)
- Family history of APKD
- End-stage renal failure
- Hypertension
ADPKD - Pathology
- PKD1 encodes polycystin 1 which regulates tubular development in kidneys
- PKD2 encodes polycystin 2 which functions as a calcium ion channel
- Polycystin complex is in cilia responsible for sensing flow in the tubule
- Disruption means reduced cytoplasmic Ca2+ → defective ciliary signalling and disorientated cell division in principal cells → cyst formation
- Mechanical compression, apoptosis of healthy tissue and reactive fibrosis → loss of renal function
- Rate of decline is dependent on growth and size of cysts
ADPKD - Symptoms (7)
- Acute loin pain
- Abdominal discomfort
- Nocturia
- Haematuria
- Hypertension
- Bilateral kidney enlargement
- UTIs and pyelonephritis
ADPKD - Differential Diagnosis (4)
- Acquired and simple cysts
- ARPKD
- Medullary sponge kidney
- Tuberous sclerosis
ADPKD - Investigations (3)
- History - family history
- Ultrasound - diagnostic if 15-39 years ≥ 3 cysts, 20-59 ≥ 2, >60 ≥ 4, <30 with family history at least 2
- Genetic testing - PKD1 or PKD2
ADPKD - Treatment (5)
- Nothing slows progression
- BP control with ACEi (Ramipril)
- Laparoscopic removal to help pain
- Nephrectomy
- Renal replacement therapy for ESRF
ARPKD - Epidemiology
- Rarer than ADPKD
- Disease of infancy
ARPKD - Cause
PKHD1 mutation on long arm of chromosome 6
ARPKD - Symptoms (3)
- Mostly present in infancy with multiple renal cysts and congenital hepatic fibrosis
- Can cause renal failure before birth → fetus has less urine → oligohydramnios (low amniotic fluid)→ potter sequence (developmental abnormalities e.g. clubbed feet, flattened nose)
- 30% develop kidney failure
ARPKD - Differential Diagnosis (4)
- ADPKD
- Multicystic dysplasia
- Hydronephrosis
- Renal vein thrombosis
ARPKD - Investigations (3)
- Ultrasound
- CT and MRI to monitor liver disease
- Genetic testing
ARPKD - Treatment (6)
- No treatment
- BP control with ACEi or ARBs
- Laparoscopic removal
- Nephrectomy
- Renal replacement therapy for ESRF
- Liver transplant
Renal Cell Carcinoma - Epidemiology
- Malignant cancer of proximal convoluted tubular epithelium
- Often asymptomatic and discovered incidentally
- 25% have metastasis at presentation
Renal Cell Carcinoma - Types
- Clear cell (80%)
- Papillary (15%)
- Chromophobe (5%)
Renal Cell Carcinoma - Symptoms (5)
- Vagure loin pain
- Haematuria
- Abdo mass
- Varicocele
- Anaemia
Renal Cell Carcinoma - Investigations (3)
- Ultrasound - 1st line
- Renal biopsy - diagnostic
- CT chest/abdo/pelvis - more sensitive than ultrasound
Renal Cell Carcinoma - Treatment
Nephrectomy or partial nephrectomy if bilateral - 1st line
Renal Cell Carcinoma - Complications (4)
Paraneoplastic changes - polycythaemia, hypertension, hypercalcaemia, Cushing’s
Nephrotic Syndrome - Description
Protein leaks due to inflammation of podocytes
Nephrotic Syndrome - Pathology
Inflammation from immune cells (IgG) → damage of podocytes → protein leakage (albumin) → increased liver activity to increase albumin → consequential increase in cholesterol and coagulation factors → reduced oncotic pressure → oedema → blood volume decrease, RAAS stimulation, exacerbation
Nephrotic Syndrome - Symptoms (5)
- Proteinuria (>3.5g/day) - damaged glomerulus is more permeable → more protein from blood into nephron
- Hypoalbuminaemia - albumin leaves blood
- Oedema (periorbital and arms) - oncotic pressure falls due to less protein in blood → lower osmotic pressure → water driven out of vessels into tissues
- Hyperlipidaemia - loss of protein = less lipid synthesis → more lipid in blood → more in urine
- Breathlessness
Nephrotic Syndrome - Causes (10)
- Primary - membranous glomerulonephritis (GN), minimal change disease, focal segmental glomerulosclerosis, membranoproliferative GN
- Secondary - diabetic nephropathy, SLE, amyloidosis, Hep B/C, myeloma, drugs
Nephrotic Syndrome - Investigations (4)
- Urine dipstick - haematuria, proteinuria
- Bloods - FBC, ESR, U&Es, creatinine
- Renal ultrasound
- Needle biopsy and microscopy - gold standard
Nephrotic Syndrome - Treatment (3)
- Steroids in children
- Diuretics for oedema
- ACEi/ARBs for proteinuria
Nephrotic Syndrome - Complications (4)
- Infections
- Thromboembolism
- Hypercholesterolaemia
- Chronic renal failure
Nephritic Syndrome - Description
Blood vessels inflamed → blood leaks out
Nephritic Syndrome - Symptoms (7)
- Haematuria - can be visible or non-visible
- Reduced GFR - hypercellular glomeruli → decreased blood flow and leaks BM → reduced filtration
- Oliguria
- AKI symptoms
- Proteinuria - <2g in 24hrs
- Oedema - periorbital, leg and sacral
- Hypertension
Nephritic Syndrome - Causes (8)
- Primary - IgA Nephropathy (most common cause), mesangiocapillary GN, diffused proliferative GN
- Secondary - post-streptococcal GN, vasculitis, SLE, Goodpasture’s, Cryoglobulinaemia
Nephritic Syndrome - Investigations (4)
- Urine dipstick - haematuria, proteinuria and RED CELL CLASTS (differentiates nephritic and nephrotic)
- Bloods - FBC, ESR, U&Es, creatinine
- Renal biopsy
- Renal ultrasound
Nephritic Syndrome - Treatment (2)
- Corticosteroids
- Hypertension treated with ACEi, salt restriction, loop diuretics (oral furosemide) and CCB (amlodipine)
Von Hippel-Lindau - Description
Rare genetic disorder - mutation of tumour suppressor gene VHL (chrom 3) 20% are de novo mutations (recent mutation)
Benign tumours and cysts in many organs and malignant tumours in certain locations
Von Hippel-Lindau - Pathology
VHL normally regulates hypoxia inducible factor (HIF) which promotes transcription of PDGF and VEGF
Von Hippel-Lindau - Tumour Locations (6)
- CNS (haemangioblastoma)
- Liver
- Lungs
- Pancreas (malignant neuroendocrine)
- Adrenals (phaeochromocytoma)
- Renal cell carcinoma (in 70% with VHL mutation)
Von Hippel-Lindau - Symptoms (4)
- Renal cell carcinoma - haematuria, flank pain, abdominal mass
- B symptoms - weight loss, fever, fatigue, night sweats
- CNS - ataxia, headaches, N&V
- Phaeochromo - headaches, sweating, palpitations, hypertension
Von Hippel-Lindau - Investigations (5)
- Screening - annual BP and abdo ultrasound
- CT head, chest and abdo
- MRI - baseline scan, tumour staging
- Bloods - FBC, U&Es, LFTs
- Renal biopsy - histology of tumour
Von Hippel-Lindau - Treatment (2)
- Surgery - once renal cell carcinoma >3cm
- Nephrectomy
Wilm’s Tumour - Description
- Affects kidneys in children (usually <5 years)
- Early tumours have 90% cure chance, worse if its metastatic
Wilm’s Tumour - Symptoms (7)
- Abdo mass
- Abdo pain
- Haematuria
- Lethargy
- Fever
- Hypertension
- Weight loss
Wilm’s Tumour - Investigations (3)
- Ultrasound - 1st line
- CT/MRI - staging
- Biopsy - diagnostic
Wilm’s Tumour - Treatment (2)
- Nephrectomy 1st line
- Chemo or radiotherapy if that doesn’t work
IgA Nephropathy - Epidemiology
- Most common cause of nephropathy worldwide
- Usually presents in childhood during GI or respiratory infection
IgA Nephropathy - Pathology
- IgA depositis in mesangium of kidney → kidney attacked by anti-glycan autoantibodies → complement pathway activation → release of pro-inflmmatory cytokines and macrophages
- Type of type III hypersensitivity so inflammation occurs as deposition site not site of formation
IgA Nephropathy - Symptoms (7)
- Haematuria
- Proteinuria
- Hypertension
- Oedema
- Oliguria
- Uraemia
- Decresed GFR (moderate-severe)
IgA Nephropathy - Investigations (3)
- Biopsy - diffuse mesangial IgA deposits, sub-endothelial and sub-epithelial deposits
- Light microscopy - mesangial proliferation
- Urine dipstick
IgA Nephropathy - Treatment (2)
- Supportive - BP control, diet, lower cholesterol
- Immunosuppression - steroids with cyclophosphamide (in induction) or azathioprine (in remission)
Minimal Change Disease - Pathology
Cytokines attack foot processes of podocytes, shrinkage/blunting of podocytes leads to protein leakage. Most common in children
Minimal Change Disease - Investigations (2)
- Renal biopsy
- Electron microscopy
Minimal Change Disease - Treatment (2)
- Corticosteroids and Cyclophosphamide
- Cyclosporine rather then Cyclophosphamide for frequent relapses
