Nephrology Flashcards
Describe the pathophysiology, presentation and management of renovascular disease
Progressive narrowing of the renal arteries with atheroma causes reduced perfusion. GFR falls but tissue oxygenation of the cortex and medulla is maintained
Progression of RA stenosis to 70% causes cortical hypoxia and microvascular damage and activation of inflammatory and oxidative pathways.
Parenchymal inflammation and fibrosis progress and become irreversible and at this point, restoration of blood flow has no benefit
Presents with hypertension, pulmonary oedema, bruits, hx of vascular disease
Manage with BP control (not ACEi/ARB), statins, good glycaemic control if diabetic, smoking cessation, exercise, low sodium diet
Angioplasty only used if rapidly deteriorating renal failure, uncontrolled HTN or flash pulmonary oedema
Define acute kidney injury and describe factors contributing to its development
‘decline of renal excretory function over hours or days, recognised by the rise in serum creatinine and drop in urine output’
Pre-Renal - Circulatory Failure/Shock - Reduced Perfusion of the Glomerulus
Renal - Cells of the Kidney
Post-Renal - Obstruction
Define glomerulonephritis
Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli that allows protein (+/- blood) to leak out into the urine
State methods of assessing kidney function and their uses and limitations
- 24hr Urine Collection (g/24h)
- Cumbersome, not routinely used in clinical practice
- Protein:Creatinine Ratio (PCR) (mg/mmol)
- Albumin:Creatinine Ratio (mg/mmol)
- Estimation of GFR
- Based on plasma creatinine concentration
- Not suitable in AKI
- Affected by muscle mass
Describe the pathophysiology, presentation and management of amyloidosis
Deposition of highly stable insoluble protein material in extracellular space in the kidney, heart, liver and gut
AA = Systemic Amyloidosis - Treat underlying source of inflammation/infection
AL = Immunoglobulin fragments from haematological conditions (e.g. myeloma) - Treat the underlying haematological condition
State common types of renal stones
- Calcium (80%)
- Calcium Oxalate Monohydrate or Dihydrate
- Calcium Phosphate
- Infection (10%)
- Struvite
- Uric Acid Stone (5%)
- Not seen on X-Ray
- Others (1%)
- Cystine, Xanthine, Silica
State functions of the kidneys
Metabolic waste excretion
Endocrine functions
Drug metabolism/excretion
Control of solutes and fluid status
Blood pressure control
Acid/base balance
State indications for renal replacement therapy
Hyperkalaemia
Acidosis
Uraemia
Fluid Overload (hypertension, pulmonary oedema)
Describe the management of UTI
Treatment with antibiotics empirically while awaiting cultures and sensitivities
Oral therapy should be used unless severely ill, vomiting or in infants <3 months
Oral - Trimethoprim, Cephalosporin, Co-Amoxiclav, Nitrofurantoin
IV - 3rd Gen Cephalosporins (Ceftriaxone) or Aminoglycosides (Gentamicin)
Describe IgA nephropathy, its diagnosis and management
Most common type of GN in adults worldwide
Proliferative
Characterised by mesangial proliferation, increased IgA production and IgA deposition
Often presents 24-48hrs after a URTI
Can present with haematuria, hypertension and proteinuria (nephritic syndrome)
Biopsy needed for definitive diagnosis
Managed with anti-hypertensives, ACEi, steroids
Describe the pathophysiology of renal stone disease
- Abnormal Urine
- Too much calcium
- Too much acid
- Hypercalciuria
- Hyperoxaluria
- Stone inhibitors (citrate, magnesium)
- Obstruction
- Congenital or Acquired
- Infection
- Particularly urease-producing organisms
- Raises urine pH
Describe the two main congenital abnormalities of the kidneys and urinary tract
- Vesico-Ureteric Reflux
- Retrograde passage of urine from the bladder into the upper urinary tract
- May present with UTI and pyelonephritis
- Can result in renal scarring
- Low-grade VUR is more likely to spontaneously resolve
- Manage with antibiotic prophylaxis or STING procedure or open ureteric re-implantation surgically
- Bladder Outlet Obstruction
- Posterior Urethral Valve
- Antenatal hydronephrosis, UTI, poor urinary stream, renal dysfunction
- Manage with valve resection, antibiotic prophylaxis, CKD care
- Pelvi-Ureteric Junction Obstruction
- Abdominal mass, pain, haematuria, UTI
- Manage with pyeloplasty
- Vesico-Ureteric Junction Obstruction
- Anatomical or functional narrowing
- Antenatal dilation, UTI, abdominal mass, pain, haematuria
- May improve or resolve spontaneously
- May need resection
Describe the medical management of chronic kidney disease
- Treatment to slow renal disease progression
- Aggressive BP control (ACEi/ARB)
- Improved glycaemic control
- Exercise
- Sodium restriction
- Treatment of renal complications
- Manage anaemia (iron, B12, folate, EPO stimulator)
- Acidosis (sodium bicarb supplements)
- Oedema (fluid/sodium restriction, diuretic)
- Bone mineral disorders (Vit D supplements, phosphate binders)
- Other
- Statins
Describe other inherited cystic disorders of the kidneys
- Von Hippel Lindau
- Autosomal dominant
- Causes multiple benign and malignant neoplasms
- Renal cysts and multifocal renal cell carcinomas
- Tuberous Sclerosis
- Autosomal dominant
- Benign hamartomas of multiple systems (brain, eyes, heart, lung, liver, skin, kidney)
- Up to 80% have renal involvement with multiple cysts, angiomyolipomas (high risk of bleeding) and renal cell carcinoma
- Replacement of renal tissue leads to kidney failure
- Medullary Cystic Kidney Disease
- Autosomal dominant
- Cysts at the cortico-medullary junction
- Causes hyperuricaemia and gout
Describe the diagnosis of UTI/Pyelonephritis
- Multistix
- Useful for children >3 years
- +ve LE & Nitrite = UTI in 90%
- Microscopy/Flow Cytometry
- If -ve for pus cells and bacteria = No UTI
- Urine Culture
- Single Organism >= 105 CFU/ml
Define nephrotic syndrome
3.5g Proteinuria per 24h (Urine PCR>300)
Serum Albumin <30
Oedema
(Hyperlipidaemia)
Describe minimal change glomerulonephritis
Non-proliferative
Most common GN in children
Presents with nephrotic syndrome
Often idiopathic, but can be secondary to malignancy
Electron microscopy shows fused podocyte foot processes
Manage with supportive care (e.g. to reduce oedema) and prednisolone
Describe membranous glomerulonephritis, its diagnosis, management and prognosis
Presents with nephrotic syndrome
Non-proliferative
Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins
Microscopic analysis shows thickened glomerular basement membrane
Immunofluorescence shows diffuse uptake of IgG
Treat underlying disease if secondary
Supportive non-immunological - ACi, statin, diuretics, salt restriction
Immunotherapy can be used if disease progresses (steroids, cyclosporin)
1/3rd spontaneously remit, 1/3rd have chronic membranous GN, the remaining 1/3rd progress to end-stage renal failure
Define chronic kidney disease and a system to classify its severity
‘kidney damage or GFR <60ml/min per 1/73m2 for three months or more’
Classified based on eGFR
Describe haemodialysis and its potential complications
Aims to remove solutes (potassium, urea) by diffusion and fluid by convection
Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction
DIffusion of solutes occurs down the concentration gradient
Access is usually through an arteriovenous fistula
Most commonly hospital-based
Standard regimen is 4 hours, 3 times a week
Problems include access complications, hypotension, cramps, fatigue, infection, dialysis disequilibrium
State risk factors for UTI
Infancy (<1 yr)
Abnormal Urinary Tract (Congenital or Other)
Female Sex
Bladder Dysfunction/Incomplete Emptying
Foreign Body (Catheter, Stone)
Diabetes Mellitus
Renal Transplant
Immunosuppression
State the range of organisms that cause UTI
Usually anaerobes and gram -ve bacteria from bowel/vagina
E.coli is the most common community organism
Staphylococcus saprophyticus and klebsiella pneumonia are other organisms involved
Describe the pathophysiology, presentation and management of diabetic nephropathy
Hyperglycaemia leads to volume expansion, intra-glomerular hypertension, hyperfiltration, proteinuria, hypertension and renal failure
Diabetic disease induces structural changes, thickening of glomerular basement membrane, fusion of podocyte foot processes and loss of podocytes
Often presents after retinopathy with proteinuria as a hallmark
Mainstay of treatment is tight glycaemic control, good BP control (with ACEi/ARB) and SGLT-2 inhibitors
Describe the pathophysiology, presentation and management of SLE
Auto-immune disease with immune complex mediated glomerular disease
Multiple autoAbs, directed against DNA, histones etc.
Form intravascular immune complexes or attach to GBM
Complement is activated leading to renal damage
Can present with elevated creatinine, proteinuria, nephritic syndrome
Treated with immunosuppression - steroids, rituximab, cyclophosphamide
Describe peritoneal dialysis and its potential complications
Uses the peritoneal membrane as a semi-permeable membrane
Catheter inserted into the peritoneal cavity and fluid is infused
Glucose is used as an osmotic agent to achieve ultrafiltration
Continuous process, home based
Requires patient to drain and refill
Complications include peritonitis, infection, hernia, loss of membrane function, glucose load
Describe rapidly progressing (cresentic) glomerulonephritis, its diagnosis and management
An aggressive form of GN
Progresses to end-stage renal failure over a few weeks if left untreated
Common Causes:
Goodpasture’s - Antibodies against glomerular basement membrane (anti-GBM), present with nephritic syndrome and haemoptysis, require high dose immunosuppression (IV Prednisolone and Cyclophosphamide)
Microscopic Polyangiitis - MPO Antibody, +ve pANCA
Granulomatosis with Polyangiitis - PR3 Antibody, +ve cANCA
Describe the emergency management of acute kidney injury
Protect Airway and Breathing
Restore Renal Perfusion
Assess for Pulmonary Oedema
Treat Hyperkalaemia if >6.5 (Calcium Chloride, IV Insulin, Salbutamol or Renal Replacement)
Treat Sepsis
Remove Offending Drugs
Correct Acidosis
Indications for RRT - Persistent Hyperkalaemia, Acidosis, Uraemia (pericarditis, encephalopathy), Toxins
Describe the clinical consequences of progressive chronic kidney disease
Albuminuria
Pruritis, Nausea, Anorexia, Weight Loss, Fatigue, Leg Swelling, Breathlessness, Nocturia, Joint/Bone Pain, Confusion
Peripheral/Pulmonary Oedema, Pericardial Rub, Rash, Hypertension, Tachypnoea, Cachexia, Pallor
Describe post-infectious glomerulonephritis, its diagnosis and management
Proliferative
Can occur after almost any infection, particularly after strep. pyogenes
Anti-body production and sub-epithelial deposition of immune complexes
Presents with oliguria, haematuria, proteinuria, oedema and hypertension
May require dialysis or antibiotics
Usually resolves over weeks, and almost always a benign prognosis
Describe the pathophysiology, presentation and management of renal cancer
Renal cell carcinoma is the most common, others include transitional cell carcinoma, sarcoma and metastases
80% are found incidentally
Systemic symptoms include night sweats, fever, fatigue, weight loss, haemoptysis
10% present with the classic triad (mass, pain, haematuria)
Initial diagnosis is made with USS, CT, MRI or renal biopsy
Manage with partial or radical nephrectomy, cryotherapy
Describe the epidemiology of renal stone disease
10-15% Lifetime Risk
Peak Incidence of 30-50 Yrs
Males > Females
Caucasian>Asian>Black>Hispanic
More common in hot, dry climates
Risk of further stone is 50% at 10 years and 90% at 30 years
Describe adult polycystic kidney disease, its presentation and management
Autosomal dominant
Most common inherited kidney disorder
Most are associated with PKD-1 gene mutation, some with PKD-2 gene mutation
These genes code for Polycystin 1 and 2, located in renal tubular epithelia and overexpressed in cyst cells, membrane proteins involved in intracellular calcium regulation
Cysts gradually enlarge, kidney volume increases and there is some compensation
eGFR falls, usually 10yrs before the kidney fails
Diagnosed with USS:
If FHx - Age 15-30, 2 Unilateral or Bilateral Cysts. Age 30-59, 2 Cysts in Each Kidney. >60, 4 Cysts in Each Kidney
If No FHx - 10 or More Cysts in Both Kidneys, Renal Enlargement, Liver Cysts
Complications: End stage renal failure, hypertension, hernias, liver/pancreas cysts
Management is supportive, BP control, treat complications and extra-renal associations
May require renal replacement therapy
Tolvaptan - Vasopressin V2 receptor antagonist, can delay onset of RRT by around 4-5yrs. S/E include hepatotoxicity and hypernatraemia
Describe the diagnostic process in acute kidney injury
Rise in serum creatinine >26micromol/L
Rise in serum creatinine >1.5x baseline
Urine output <0.5ml/kg/h for >6 consecutive hours
- CKD or AKI?
- History and Exam (Sepsis, Haemoptysis, Rhabdo)
- Drugs
- Urinalysis
- Renal USS
- Exclude obstruction
- Info on kidney size
- GN Screen
- ANCE, ANA, Ig, Complement, aGBM, Urine Bence Jones Protein
- Other Blood Film
Describe the presentation of renal stones
Incidental
Pain (colic, radiates from loin to groin, cannot settle, unable to stay still)
Haematuria
UTI
Sepsis
Investigate with CT, Bloods (U&Es, CRP, FBC), Urinalysis, Urate, Calcium
Describe other inherited renal disease
- Alport’s Syndrome
- Usually X-Linked
- Abnormality in Collagen IV (found in basement membranes, so associated with anti-GBM disease)
- Presents with haematuria, proteinuria and progressive renal insufficiency
- Results in renal failure
- Often associated with sensorineural hearing loss
- Fabry’s Disease
- X-Linked
- Lysosomal storage disorder due to deficiency of alpha-glucosidase
- Causes proteinuria, end-stage renal failure, lipid deposits in urine
- Manage with IV enzyme replacement therapy
Describe the pathophysiology and clinical presentation of pyelonephritis
UTI refers to infection anywhere along the urinary tract, from kidney to urethra
Pyelonephritis specifically refers to infection of the kidney/renal pelvis
Presents with dysuria, frequency, urgency, suprapubic pain, haematuria, fever, chills/rigor, flank pain, costovertebral angle tenderness, nausea, vomiting
State the aetiology of acute and chronic glomerulonephritis
Group A Strep
Systemic Inflammatory Diseases (SLE, RA)
Drugs (e.g. NSAIDs)
Diabetes
Hypertension
Amyloidosis
Describe the short and long-term consequences of renal transplantation
Far better outcome than dialysis
Cadaveric waiting list of approx. 3 years
- Pros
- No dialysis
- Better level of renal function
- Can live much more independently
- Better life expectancy
- Better fertility
- Cons
- Immunosuppressive medication for duration of transplant
- Increased CV risk
- Increased infection
- Post-transplant diabetes
- Skin malignancies and others
- Risk of acute/chronic rejection, surgical bleeds
Immunosuppression with monoclonal antibodies, calcineurin inhibitors antimetabolites, glucocorticoids
Describe the pathophysiology, presentation and management of bladder cancer
Majority are transitional cell carcinomas
Can be squamous carcinomas and adenocarcinomas
Classically presents with painless frank haematuria
Diagnosed with flexible cystoscopy
Manage with mitomycin, chemotherapy, radical cystectomy, radiotherapy
If metastatic, treat with M-VAC chemotherapy (methotrexate, vinblastine, doxorubicin, cisplatin)
Describe the pathophysiology, presentation and management of prostate cancer
Most are primary adenocarcinoma, usually arising in the peripheral zone of the prostate
May be asymptomatic or present with painful/slow micturition, UTIs, haematuria, retention, lymphoedema
Metastatic features may include bone pain and renal failure due to ureteric obstruction
Diagnosed by digital rectal examination, prostate-specific antigen and trans-urethral guided needle biopsy
Note that PSA is tissue, not tumour specific and tends to rise with age
Manage localised disease with surveillance, radiotherapy, radical prostatectomy, cryotherapy
For advanced cancer, androgen ablation therapy (medical or surgical castration), chemotherapy, radiotherapy
Describe the pathophysiology, presentation and management of testicular cancer
Most are germ cell tumours (seminoma, teratoma) but can be stromal (leydig or sertoli) or lymphoma
Majority present as a painless lump, or may be found after incidental trauma
Investigate with scrotal USS, alpha-fetoprotein, Beta-hCG, LDH
Treat with radical orchidectomy, chemotherapy, nodal radiotherapy
Describe the management of renal stone disease
Analgesia (NSAIDs, e.g. Diclofenac)
Small stones are likely to pass spontaneously
Larger stones or if non-remitting pain, may require medical expulsive therapy (alpha-blocker - tamsulosin)
Surgical options include Extracorporeal Shockwave Lithotripsy, Ureteroscopy with Basket Extraction or Percutaneous Nephrolithotomy
