Abdominal pain- kidneys Flashcards
The 5 functions of the kidney
• Excretion of toxins
• Maintenance of fluid homeostasis
• Maintenance of electrolyte homeostasis
• Regulation of acid base balance
• Production of hormones: Vitamin D, erythropoietin and renin
Nephron: Afferent and efferent arteriolr, Glomerular capillaries
• Afferent arteriole: receives blood from the systemic circulation and helps regulate pressure in the glomerulus
• Glomerular capillaries: receives blood from the afferent arteriole. Fluid and electrolytes are forced across the filtration surface into the Bowmans capsule which receives the filtrate
• Efferent arteriole: outflow from the glomerular capillaries, also helps to regulate pressure in the glomerulus
Nephron: Peritubular capillaries, renal tubules, collecting ducts
• Peritubular capillaries- involved in the transfer of substances with the renal tubules (reabsorption and secretion)
• Renal tubules: can be divided into the proximal tubule, Loop of Henle and the distal tubules. Involved in the transfer of substances with the peritubular capillaries (reabsorption and secretion)
• Collecting ducts: involved in the reabsorption of water and the drainage of filtrate away from the nephron
Factors which act upon the glomerulus (1-3)
• Resistance in the afferent arteriole: reduced by factors such as prostaglandins i.e. PGE2 which promote vasodilation
• Pressure in the glomerular capillaries: influenced by resistance in the afferent and efferent arterioles
• Resistance in the efferent arteriole: resistance is increased by factors such as angiotensin II which promote vasoconstriction
Factors which act upon the glomerulus (4-6)
• Pressure in the Bowmans capsule: increased resistance to outflow, for instance due to lower urinary tract obstruction, reduced glomerular filtration
• Permeability of filtration surface: reduced permeability, for instance due to glomerulonephritis will reduce glomerular filtration
• Glomerular filtration is maintained by ensuring resistance in the efferent arteriole is greater than resistance in the afferent arteriole. Glomerular filtration can only occur if there is sufficient (hydrostatic) pressure in the glomerular capillaries
Conditions which reduce the hydrostatic pressure in the glomerulus
Hypotension, renal artery stenosis, ACEi (loss of efferent arteriolar constriction), NSAID’s (loss of afferent arteriole dilation)
Conditions which increase the hydrostatic pressure in the Bowmans capsule
Urinary tract obstruction
Glomerular filtration and AKI
Loss of glomerular filtration is the key symptom in an AK and causes circulation volume overload, hyperkalaemia and acidosis. Causes of reduced glomerular filtration include hypotension, some drugs and urinary tract obstruction
Tubular secretion in the kidneys
Includes potassium, hydrogen ions, buffers, creatinine and some drugs. Tubular secretion plays an important role in potassium and acid base homeostasis and is important in the pharmacology of some drugs.
Potassium in the kidney
• Reabsorption of potassium in the proximal tubule
• Reabsorption of potassium in the ascending loop of Henle, for instance via the sodium potassium chloride co-transporter (target for loop diuretics)
• Secretion of potassium in exchange for sodium in the distal tubule (stimulated by aldosterone)
Potassium in the body
• Whole body potassium does not equate to serum because most bodily potassium is stored within cells
• Serum levels are determined by cellular uptake and release
• Hormones which cause cellular storage: insulin, catecholamine
• What promotes cellular release: acidosis
Acid-base balance in the kidneys
The glomerular filtration of acids from the blood and the tubular reabsorption of bicarbonate and secretion of hydrogen ions
Kidney- drugs
- Nephrotoxic drugs: Gentomycin- due to a variety of mechanisms including tubular epithelial damage
- Which drugs reduce glomerular filtration: ACEi, NSAID’s, antihypertensives and diuretics
- Opiates like morphine and some anticoagulants like low molecular weight heparin rely on the kidneys to be deactivated or excreted
- Nitrofurantoin and diuretics like furosemide rely on glomerular filtration and tubular secretion in order to work.
Function of the kidneys: synthesis of hormones
• Erythropoietin- done in the peritubular capillary cells of the renal cortex, produced in response to hypoxia and stimulates red blood cell production
• 1,25-hydroxyvitamin D3- plays an important role in calcium and phosphate homeostasis. 25-hydroxyvitamin D3 is filtered at the glomerulus and delivered to the tubular epithelium where it undergoes 1 hydroxylation to produce 1,25-hydroxyvitamin D3 which is the active hormone.
• Renin: its released by cells in the juxtaglomerular apparatus in response to hypotension, sympathetic activation and reduced sodium delivery to the macula densa in the distal tubule.
• Loss of endocrine function can contribute to anaemia and renal bone disease, more associated with CKD
Causes of AKI
• Urinary tract obstruction (lower abdominal pain, palpable urinary bladder, renal angle tenderness)
• Sepsis (fever or features of infection and signs of an abnormal host response such as new confusion, increased respiratory rate, tachycardia and hypotension)
Predisposing factors for AKI
• Vasculopathy (absent peripheral pulses, palpable abdominal aortic aneurysm)
• Frailty (walking sticks, cachexia)
• Stigmata of diabetes mellitus (injection or blood glucose test site marks, cataracts, obesity (type 2 diabetes), skin thickening, foot ulcers, special footware and mobility aids, fungal infections)
Complications of an AKI
• Fluid overload (raised JVP, peripheral oedema, bibasal crackles and a third heart sound).
• Acidosis (Kussmaul breathing pattern)
Causes of an AKI
• Pre-renal – Renal hypoperfusion due to relative hypotension (sepsis, dehydration, heart failure) or loss of hydrostatic pressure at the glomerulus (often drug mediated). Sustained renal hypoperfusion will lead to acute tubular necrosis.
• Intrarenal – Glomerular pathology (eg autoimmune disease, drugs, infection, primary glomerulonephritis - uncommon), tubular pathology (eg acute tubular necrosis - for instance due to a prolonged episode of relative hypotension), interstitial disease (drugs, autoimmune disease, infiltration).
• Post renal – Urinary tract obstruction at whatever level; ureteric, bladder outflow, urethra.
Classifications of an AKI- stage 1
Creatinine rise of 26 micromol or more within 48 hours. OR. Creatinine rise of 50-99% from baseline within days. OR. Urine output <0.5mL/kg/h for more than 6 hours
Classifications of AKI: stage 2
100-199% creatinine rise from baseline within 7 days. OR. Urine output <0.5mL/kg/hour for more than 12 hours
Classification of AKI: stage 3
200% or more creatinine rise from baseline within 7 days. OR. Creatinine rise to 3.54 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days. OR. Urine output <0.3 mL/kg/hour for 24 hours or anuria for 12 hours
Complications of stage 3 AKI
• Fluid overload – On clinical examination, look for peripheral oedema, bibasal crepitations suggestive of pulmonary oedema, a raised JVP and a third heart sound
• Acidaemia – This can rapidly be excluded with a venous blood gas. A laboratory bicarbonate sample may also be helpful.
• Hyperkalaemia - This can rapidly be excluded with a venous blood gas, and confirmed on a laboratory sample.
Investigations for an AKI
• Bedside: urine dip to assess for albuminuria or haematuria which suggests a glomerular cause. Venous blood gas for estimation of serum potassium and acid base status
• Lab tests: FBC, U&E’s, LFT and bone profile to assess for anaemia, infection, hyperkalaemia, hypocalcaemia and hyperphosphataemia. Check creatinine kinase if history of falls to exclude rhabdomyolysis
• Imaging: USS kidney-ureters-bladders
Second line investigations for an AKI
• Quantification of albumin:creatinine ratio if there is evidence of proteinuria
• Myeloma screen
• Autoantibody profile (ANCA, anti-GBM and anti-dsDNA and complement levels to assess for systemic processes like vasculitis
• Virology screen- rarely AKI is associated with HIV and hepatitis, screen is required if the patient needs dialysis
• Renal biopsy
How best to monitor changes in AKI
In AKI there is a lag between improvement in glomerular filtration and the fall in serum creatinine. Raw trends in serum creatinine and urine output are therefore better indicators of changes in renal function in AKI
Approach to hyperkalaemia
1.Establish if there is myocardial toxicity by looking at his ECG - tented T wave and wide QRS complexes
2. Stabilise the myocardium if necessary with calcium gluconate
3.Reduce serum potassium levels by driving potassium in to cells with salbutamol nebulisers and IV insulin with glucose
4.Promote removal of potassium if feasible and appropriate, for instance by supporting urine output with intravenous fluids, or by seeking help early for consideration of renal replacement therapy if poor urine output. Consider dialysis
5.Correct underlying cause
6. Ensure subsequent follow up and monitoring of potassium
Distinguishing an AKI from a CKD
• An AKI is less than 4 weeks
• A discreet insult suggests AKI, a history of progressive malaise over several months with abnormal kidney function suggests CKD
• Creatinine trends over a number of days- renal function tends to improve in AKI
• Hypocalaemia and Hyperphophataemia imply CKD
• Ultrasound- small kidneys with kidney disruption suggest CKD
Treatment for AKI is generally supportive
