Week 14 Renal Flashcards
Chronic kidney disease, measures, risk factors, acc prog, management. (5)
Chronic kidney disease (CKD) is a reduction in kidney function or structural damage (or both) present for more than 3 months. (eGFR) of less than 60 mL/min/1.73 m2.
Measures:
CKD is classified based on the underlying cause, GFR, and proteinuria category. Albumin:creatinine ratio (ACR).Use reagent strips to test for haematuria.
Risk factors:
Diabetes, hypertension, previous AKI, cardiovascular disease, structural renal tract disease, recurrent renal calculi or prostatic hypertrophy, systemic lupus erythematosus, gout, hereditary kidney disease, haematuria or proteinuria, African, African-Caribbean or Asian family origin, chronic use of NSAIDs, untreated urinary outflow tract obstruction.
Accelerated progression (av of 3gfrs over 90days): A sustained decrease in GFR of 25% or more and a change in GFR category within 12 months or a sustained decrease in GFR of 15 ml/min/1.73 m2 per year.
Management:
Offer dietary advice about potassium, phosphate, calorie and salt intake appropriate to the severity of CKD. Exercise, no smoking. Antihypertensives, RAS antagonists, antiplatelets/anticoagulants. Ace/arbs for kids to.
Pharmacotherapy for CKD (6)
Most require blood pressure control. If ACR >70mg/mmol aim for <130/80 mmhg. If <70mg/mmol aim for <140/90 mmhg. For children it’s 50%tile for height. Usually ACE/ARBs.
RAS antagonists are given but don’t combine them. Must measure eGFR and serum potassium before and 1-2 weeks after or with dose change. X give if K+ >5mmol/L. Sodium zirconium, cyclosilicate and patiromer.
Give antiplatelets if risk of CVD.
Manage iron <110/L or symptomatic. Iron therapy or ESA treatment.
Also might encounter hyperparathyroidism, osteoporosis. X give CKD vit C, folic acid nor androgens.
Might need phosphate binders for hyperphosphataemia, eg calcium acetate.
Acute kidney injury
The causes of acute kidney injury can be divided into pre-renal (for example hypovolaemia, decreased cardiac output), intrinsic renal (for example nephrotoxic drugs, interstitial nephritis), and post-renal (for example renal stones, bladder outflow obstruction from prostate enlargement).
Measurement:
A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days.
A fall in urine output to less than 0.5mL/kg/hour for more than 6 hours.
25% or greater fall in eGFR in children and young people within the past 7 days.
Risk factors:
chronic kidney disease, heart failure, liver disease, history of acute kidney injury, oliguria (urine output less than 0.5 ml/kg/hour), NSAIDs/ACE/ARB/Diuretics/Aminoglycosides, hypovolaemia, sepsis, urinary obstruction, nephritis, haematological malignancy, renal transplant.
Management:
Urologist referral for: pyonephrosis, an obstructed solitary kidney, bilateral upper urinary tract obstruction, complications of acute kidney injury caused by urological obstruction.
Nephrostomy or stenting, renal replacement therapy.
Prescribing in renal impairment
What medications to avoid with kidney disease:
Pain medications also known as nonsteroidal anti-inflammatory drugs (NSAIDs) Proton pump inhibitors (PPIs) Cholesterol medications (statins) Antibiotic medications Diabetes medications Antacids Herbal supplements and vitamins Contrast dye Antivirals Some chemotherapy Some ulcer medicines
May increase the risk of AKI: angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, and diuretics.
Defining hypertension stages, masked and white coat (5)
Stage 1 hypertension - BP in surgery/clinic is ≥140/90 mm Hg
Stage 2 hypertension - BP in surgery/clinic is ≥160/100 mm Hg but less than 180/120 mm Hg
Stage 3 or severe hypertension - systolic BP in surgery/clinic is 180 mm Hg or higher or diastolic BP is 120 mm Hg or higher.
Masked hypertension - BP in surgery/clinic is less than 140/90 mm Hg but average ABPM or HBPM readings are higher.
White coat effect - a discrepancy of more than 20/10 mm Hg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis.
Hypertensive crisises (2)
Accelerated (also known as malignant) hypertension: this is a syndrome characterised by severe hypertension (eg, systolic >200 mm Hg, diastolic >130 mm Hg) accompanied by end-organ damage - eg, encephalopathy, dissection, pulmonary oedema, nephropathy, eclampsia, papilloedema and/or angiopathic haemolytic anaemia. Accelerated hypertension needs urgent (same-day) assessment and immediate treatment to reduce the BP within minutes to hours. This is also termed hypertensive emergency.
Hypertensive urgency: a systolic blood pressure (SBP) ≥180 mm Hg or a diastolic blood pressure (DBP) ≥120 mm Hg without impending end-organ damage. Treatment should safely reduce BP over a few days. Repeat BP measurement within 7 days.
Causes of secondary HTN (5)
Secondary hypertension is commonly caused by renal disease, endocrine conditions or pregnancy:
Renal disease is the most common: This may be intrinsic renal disease - glomerulonephritis, polyarteritis nodosa, systemic sclerosis, chronic pyelonephritis, or polycystic kidneys. or renovascular disease- atheromatous or fibromuscular dysplasia.
Endocrine disease: Cushing's syndrome Conn's syndrome Thyroid dysfunction Phaeochromocytoma Acromegaly Hyperparathyroidism
Coarctation of the aorta.
Obstructive sleep apnoea.
Pre-eclampsia and hypertension in pregnancy.
Pharmacological substances and toxins - eg, alcohol, cocaine, amfetamines, antidepressants, the combined oral contraceptive (COC) pill, ciclosporin, tacrolimus, erythropoietin, adrenergic medications, decongestants containing ephedrine and herbal remedies containing licorice or ginseng.
Investigations to manage secondary HTN (6) (2)
Assess for target organ damage:
Test for haematuria
Urine albumin:creatinine ratio (to test for the presence of protein in the urine).
HbA1C (to test for diabetes).
Electrolytes, creatinine, and estimated glomerular filtration rate (to test for chronic kidney disease).
Examine the fundi (for the presence of hypertensive retinopathy).
Arrange for a 12-lead electrocardiograph to be performed (to assess cardiac function and detect left ventricular hypertrophy).
Consider the need for specialist investigations in people with signs and symptoms suggesting target organ damage or a secondary cause of hypertension.
Assess cardiovascular risk.
Arrange measurement of serum total cholesterol and high-density lipoprotein (HDL) cholesterol.
Estimate the person’s 10-year risk of developing cardiovascular disease (CVD) using the QRISK assessment tool.
Glomerulonephritis
Glomerulonephritis is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name.
It may present with isolated haematuria and/or proteinuria; or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease.
Blood tests for glomerulonephritis (5)
Blood culture - This is helpful if the physician suspects infection as the underlying cause of the nephritic syndrome.
Antinuclear antibody (ANA) titre - ANA is commonly positive in patients who have an underlying autoimmune disease, so this test is useful if the physician suspects an underlying autoimmune disease as the cause of the presenting nephritic syndrome. If positive, then the physician may order additional tests to determine which autoimmune condition is the cause and how best to treat it.
Antiglomerular basement membrane (anti-GBM) antibody - If positive, this is highly indicative of Goodpasture’s syndrome and can be used to guide treatment.
Antineutrophil cytoplasmic antibody (ANCA) - If positive, this indicates that there is likely an underlying vasculitis that may be causing the acute nephritic syndrome.
Serum complement (C3 and C4) - Complement factors bind to antibodies to form immune complexes and a decreased serum complement level could indicate that the complement is being consumed at a higher rate due to the formation of immune complexes leading to deposition in the glomerulus of the kidney.
Acromegaly (4)
Excessive GH after growth plates have closed.
Typically shows enlarged hands and feet. Can be forehead, jaw or nose. Joint pain, thicker skin, deep voice, visual issues and HTN.
Most commonly because of pituitary adenoma.
Give surgery, somatostatin analogues or GH receptor antagonists.
Fibromuscular dysplasia (3)
One or more artery to be maldeveloped- risk stenosis, aneurysms, dissections. If reduces blood flow = symptomatic. Most commonly renal arteries. Control HTN is goal.
Polycystic kidney disease (4)
Autoimmune dominant (genes PKD1,2,3) or recessive (PKHD1) disorder of renal tubes leading to developing with cysts, The cysts can also be in the liver, seminal vesicles and pancreas.
Associated with aortic root aneurysm and circle of Willis. Can result in RAAS activated HTN.
Signs- HTN, headaches, abdominal pain, haematuria, polyurea.
Renal replacement therapy.
Systemic sclerosis/scleroderma
Autoimmune rheumatoid disease with excessive production of collagen leading to fibrosis. Affects elbows and knees. If diffuse, also torso and visceral organs.
Signs- crest syndrome: calcinosis, Raynaud, oesophageal issues, sclerodactyly, telangiectasia. Also hard skin, scarring, visible vessels, fat/muscle wasting, itchy skin.
Treat:
Naproxen for pain. Nifedipine for Raynaud’s, prostacyclin analogue for hand ulcers and pulmonary htn, methotrexate and cyclosporine for tight skin, penicillamine for thick skin. ACE for htn, cyclophosphamide for pulmonary alveolitis.
Polyarteritis nodosa (4)
Systemic necrotising vasculitis of medium vessels. Usually kidneys, rarely lungs. Small aneurysms give Rosary sign. Sometimes associated with Hep B/C.
Symptoms:
Rash, ulcers, nodules, palpable purpura and livido reticularis (mottled lace), mononeuritis multiplex, HTN, testicular pain.
Risk stroke, HF, pericarditis, necrotic bowel or perforation.
Treat with prednisone and cyclophosphamide. Treat any Hep B also.
Nephritic syndrome
Nephritic syndrome is haematuria, elevated blood pressure, decreased urine output and oedema.
Other signs are hyperlipidaemia, eventually azotaemia(inc urea and creatinine), blurred vision, brown urine, pyuria, HTN.
Causes are inflammatory= thrombotic, infective or autoimmune. IgA nephropathy (commonly with URTI), post strep glomerulonephritis, Henoch schonlein purpura, haemolytic uremic syndrome (typically E.coli). Adults = Goodpasture's, SLE, infective endocarditis, cryoglobulinemia, Wegener's granulomatosis.
Treatment:
Bed rest
Follow a low in salt and potassium diet and avoid liquids with meals
High blood pressure medications or diuretics
Some cases may require kidney dialysis.
