Kidney Flashcards
Name the retro-peritoneal adominal viscera
SAD PUCKER S=suprarenal (adrenal) glands A=Aorta/IV D=duodenum (except duodenal cap- first 2cm) P=Pancreas (except tail) U= Ureters C= colon (ascending and descending) K=Kidneys E=(O)esophagus R=Rectum
The rest are intra-peritoneal
At what spinal levels do the kidneys usually lie within
T12 to L3. Right kidney usually lower due to liver. Usually 3 vertebrae in length
Layers of fascia and fat around kidneys (deep to superficial)
Renal capsule – Tough fibrous capsule.
Perirenal fat – Collection of extra-peritoneal fat.
Renal fascia – Encloses the kidneys and the suprarenal glands.
Para-renal fat – Mainly located on the posterolateral aspect of the kidney.
Arterial supply and venous drainage of the kidneys
Arterial supply:
Renal arteries from abdominal aorta
Splits into: segmental -> interlobar -> arcuate -> 90 degrees interlobular arises -> afferent arterioles
Venous drainage:
Left and right renal veins
Define nephrotic syndrome
- presence of proteinuria (>3.5 g/24 hours)
- hypoalbuminaemia (<30 g/L),
- peripheral oedema
Nephrotic syndrome-associated diseases
Primary
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Secondary Amyloidosis SLE Hep B and C (rare) Diabetic nephropathy Malignancy
Reason for proteinuria, hypoalbuminaemia and oedema
proteinuria is a result of damage to the glomerular resulting in ability for protein to squeeze into nephron. The worse the protein loss the more likely nephrotic syndrome
Hypoalbuminaemia due to urinary loss of albumin. Liver compensates by synthesis of more albumin and other proteins in particular lipoproteins hence lipid abnormalities (hypercholesterolaemia)
oedema is due to a combination of a decrease in oncotic pressure from the hypoalbuminaemia, as well as a primary renal sodium retention in the collecting tubules
Drugs associated with nephrotic syndrome
Pamidronate Lithium Gold Penicillamine NSAIDS
Causes of glomerulonephritis
Systemic lupus erythematosus
Rheumatoid arthritis
Infections
Drugs (Penicillamine, gold, heroin, NSAIDs, Cyclosporin)
Metabolic disorders (Diabetes, HTN, thyroiditis)
Malignancy (lung and colorectal cancer, melanoma, and Hodgkin’s lymphoma)
Pathophysiology of glomerulonephritis
cellular immune response results in infiltration of mononuclear inflammatory cells (lymphocytes and macrophages)
humoral immune response leads to immune deposit formation and complement activation in glomeruli.
Injury usually occurs as a consequence of the activation and release of a variety of inflammatory mediators
Common signs and symptoms of glomerulonephritis
Haematuria Oedema HTN Oliguria Anorexia Nausea Malaise Weight loss Fever Skin rash
Risk factors of glomerulonephritis
- Group A beta-haemolytic Streptococcus
- Respiratory infections
- GI infections
- Hep B, C
- HIV
- SLE
- Infective endocarditis
What is minimal change disease?
Most common form of nephrotic syndrome in children.
Characteristics only seen under an electron microscope (can see foot process effacement/thinning)
Cause of minimal change disease
Idiopathic (primary) Secondary: Drugs (NSAIDs, lithium, bisphosphonates) Malignancy (Leukemia, Lymphoma) Infection (Syphillis, HIV, Hepatitis)
Treatment of minimal change disease
Prednisolone Fluid restriction Low salt diet Albumin and Furosemide Corticosteroid sparing therapy (Ciclosporin)
Amyloidosis
Group of rare yet serious disease characterised by deposits of amyloid protein.
Amyloid is a description of proteins which have folded abnormally and then collected together.
Classifications of amyloidosis
Primary amyloidosis (AL): Aetiology unknown
Secondary amyloidosis (AA): 2 to RA, PA, ankolysing spondylitis, chronic infections, IBD
Familial Mediterranean fever
Tumour necrosis factor receptor-associated periodic fever syndromes
Muckle-Wells syndrome
Hyper-IgD syndrome
Inherited amyloidosis (AF):
Mutations of transthyretin leading to progressive cardiomyopathy or progressive neuropathy or both
Mutation of fibrinogen A alpha-chain leading to renal involvement
Mutation of apolipoprotein A
Mutation of lysozyme
Senile amyloidosis (SSA)
Signs and symptoms of amyloidosis
Lower extremities oedema Periorbital purpura Raised JVP Macroglossia (enlarged tongue in primary) Fatigue Weight Loss SOBOE
Investigations for amyloidosis
Urine fixation: light chain protein in the urine is suggestive of multiple myeloma and amyloidosis.
Serum fixation: Presence of monoclonal Ab
Immunoglobulin free light chain assay: abnormal lambda to kappa ratio
Definition of diabetic kidney disease (DKD)
Macroalbuminuria (Alb:Creat ratio >34mg/mmol)
or
Microalbuminuria (3-34mg/mmol) + associated retinopathy or T1DM >10 years.
DKD pathophysiology
Hyperglycaemia and HTN cause glomerular mesangium expansion via increase mesangial growth.
Works by:
- PDGF and transforming growth factor (TGF-b) stimulate collagen and fibronectin synthesis and decreased matrix degradation.
- Glucose binds to proteins forming advanced glycation end products (AGEs)
- AGEs crosslink and activate downstream cytokines such as TGF-b.
- AGEs modify or impair the function of the proteins (such as laminin and type IV collagen).
- Results in increase in permeability of glomerular basement membrane.
Signs and Symptoms of DKD
HTN Oedema Retinal findings: dot and blot haemorrhages, microaneurysms (background retinopathy), and/or neovascularisation (proliferative retinopathy). Poor vision Numbness or pain in lower extremeties Foot ulcers, Charcot joints
Investigations to order for DKD
Urinalysis (Proteinuria)
Urinary creatinine to albumin ratio: elevated
Serum Creatinine (GFR estimation): elevated. GFR raised in patients with CKD 1, normal in CKD 2, low in CKD 3-5
Kidney ultrasound:
normal-to-large kidneys with increased echogenicity; may show hydronephrosis if vesiculopathy and/or obstruction is superimposed
Management of type 1 DKD, not on dialysis
Insulin lipro & Insulin glargine
ACEi, (add more anti hypertensives depending on BP)
Statin,
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation
Management of patient on dialysis
Insulin lipro and Insulin glargine
(Can add sitagliptin or glipizide for T2DM)
ACEi, (add more anti hypertensives depending on BP)
Statin,
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation
If all else fails consider pancreas, kidney transplant.
Management of type 2 DKD not on dialysis
Metformin or glipizide or sitagliptin or repaglinide
(Insulin lipro and insulin glargine can be added as well)
ACEi or ARB (add more anti hypertensives if needed)
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation
What is pyelonephritis?
Infection of the kidneys resulting in inflammation of the renal parenchyma, calices and pelvis.
Major causative pathogens of pyelonephritis
Gram negative E.coli (60-80% of uncomplicated) Proteus Mirabilis (15%) Klebsiella (20%) Pseudonomas, Enterobacter species
Gram positive (less common) Enterococcus faecalis, Staphylococcus saprophyticus, and S aureus
Signs and symptoms of pyelonephritis
Fever
Vomiting & Nausea
Flank pain costovertabral angle tenderness.
Dysuria, frequency or urgency.
Risk factors for pyelonephritis
Frequent sexual intercourse UTI Diabetes Catheter, Calculus (stone) Immunosuppressive state Pregnancy
Investigation to order for pyelonephritis
Urinalysis: WBC >10, RBC >5 Gram stain (Most common gram negative rods) Urine culture >100,000 CFU/ml FBC: Raised leukocytes ESR, CRP elevated
Management of pyelonephritis
On assumption: Empirical antibiotic
Once culture has been grown used sensitive antibiotics
Nephrolithiasis (kidney stones)
Stones in the urinary system usually in response to elevated levels of urinary solutes such as calcium, uric acid, oxalate, and sodium, as well as decreased levels of stone inhibitors such as citrate and magnesium
Risk factors for nephrolithiasis
High protein or salt intake
Male sex (ratio of 3:1 male to female)
Dehydration
Obesity
Signs and symptoms
Acute severe flank pain. Radiates to ipsilateral groin Nausea and Vomiting Haematuria Testicular pain Urinary frequency/ urgency
Management of nephrolithiasis
non pregnant, acute: Hydration, pain control , anti-emetic. Abx (Trimethoprim or Nitrofurantoin) Surgical decompression Alpha blocker: (Tamsulosin, Afluzosin) Surgical removal
Non pregnant, ongoing,uric acid stone:
Alkalinisation (Potassium citrate, Sodium Bicarbonate) with or without allopurinol
Non pregnant, ongoing, hypercalcuria:
chlortalidone
hydrochlorothiazide
indapamide
For the rest see BMJ
Cystitis
Infection of the bladder mainly affects young, sexually active women.
Causative organism of cystitis
E.Coli (80%)
Staphylococcus saprophyticus, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas, Enterococcus, Enterobacter, and group B streptococci.
Pathophysiology of cystitis
E coli or other bacteria that are normally found in the GI tract or vagina can be introduced into the urethra. This may happen during sexual intercourse, or through gradual colonisation of the adjacent tissues. Bacteria may also be introduced into the normally sterile urinary tract through instrumentation, as in cystoscopy or use of a urinary catheter
Signs and symptoms of cystitis
Dysuria
Suprapubic pain
Urgency
Frequency
Risk factors of cystitis
Frequent sexual intercourse Hx of UTI Congenital abnormalities Urinary catheter Diabetes Age Pregnancy Spinal injury Immunodeficiency Uncircumcised
Investigations to order if suspecting cystitis
Pregnancy test
Urinalysis: Leukocyte esterase, nitrites, haemoglobin
Urine microscopy: RBCs, WBCs (>10), bacteria
Urine culture with sensitivity: 10^3 CFU/mL
Treatment similar to UTI treatment
