Name 6 diseases that affect the kidney that are associated with hypocomplementemia.
Hypocomplementemia in glomerulonephritis is most often due to increased complement consumption. In these cases, immune deposits cause complement consumption at a greater rate than they can be synthesized. Other less common causes of hypocomplementemia are hereditary complement deficiency and the presence of circulating factors that promote complement activation.
Hypocomplementemia can occur with the following conditions:
- Lupus nephritis
- Subacute bacterial endocarditis
- Membranoproliferative glomerulonephritis (MPGN)
- Post-streptococcal glomerulonephritis
- Cryoglobulinemic glomerulonephritis
- Atheroembolic renal disease
- Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura.
How can you determine if a 24 hour urine collection is complete?
To determine adequacy of a 24 hour urine collection, one must look at the total amount of creatinine excreted in the collection period.
Males should excrete 200 umol/kg of creatinine per 24 hours and females should excrete 150 umol/kg/24 hours.
A 70 kg male performs a 24 hour urine collection. The lab report reveals:
Volume: 2.5 L
Creatinine: 34 mmol
Protein: 240 mg
Do you think this patient has abnormal protein excretion? Why?
This patient should have produced:
70 kg * 200 umol/kg = 14 mmol of creatinine in the 24 hour collection.
Since his collection had 34 mmol of creatinine, this represents an overcollection. Therefore, the protein measured is an overestimate of his true 24 hour protein excretion. One could estimate that his true protein excretion rate would be closer to:
(14 / 34) * 240 mg = 99 mg per day, which would fall within the normal range.
Where do the following diuretics act along the nephron?
Loop diuretics act in the thick ascending limb of the loop of Henle, thiazide-type diuretics act in the distal tubule and connecting segment (and perhaps the early cortical collecting tubule) and potassium-sparing diuretics act in the aldosterone-sensitive principal cells in the cortical collecting tubule.
- Acetazolamide is a carbonic anhydrase inhibitor that acts in the proximal convoluted tubule
- Furosemide blocks the NaK2Cl channel in the thick ascending limb of the loop of Henle
- Hydrochlorothiazide inhibits the NaCl cotransporter in the distal tubule
- Spironolactone competitively inhibits the aldosterone mineralocorticoid receptor in the cortical collecting duct
- Amiloride blocks ENaC (epithelial sodium channel) in the cortical collecting duct
How can you differentiate acute from chronic renal failure? Explain this in terms of history, physical examination and laboratory tests.
In terms of history, one must determine whether previous serum creatinines are available or if there is any history of any systemic diseases that may be associated with renal involvement. Often, one must take the time to call other physicians or hospitals to get old creatinine values.
When it seems that one is dealing with acute renal failure, then there needs to be an assessment for pre-renal, renal, or post-renal causes.
On physical examination, one should look for evidence of a pre-renal cause of renal insufficiency. Hypovolemia would be suggested by features of decreased extracellular fluid volume such as a low JVP, dry mucous membranes or postural tachycardia, or hypotension. Pre-renal disease can also be due to conditions such as congestive heart failure or cirrhosis, so one should also perform a careful cardiac exam and look for stigmata of chronic liver disease.
Post-renal failure can be seen in bladder outlet obstruction, so one could feel for a palpable bladder. Intrinsic renal disease can develop acutely due to systemic disease with renal involvement. One can look for features of some of these systemic conditions which might include rashes, active joints, alopecia, oral/nasal ulcers, peripheral neuropathy, or a murmur from endocarditis.
In terms of lab data, urinalysis is critical. One may see casts that will helpful in terms of diagnosis: RBC casts for glomerulonephritis, WBC casts in acute interstitial nephritis, and heme granular casts in acute tubular necrosis. In chronic renal disease, one may see waxy or broad casts.
Chronic renal failure may also be associated with anemia, metabolic acidosis, hypocalcemia, and hyperphosphatemia. These may not be entirely reliable; however, as anemia can develop acutely in patients with conditions such as lupus or vasculitis, and hypocalcemia/hyperphosphatemia can be seen in conditions such as tumour lysis syndrome.
On ultrasonography, small kidneys with cortical echogenicity would suggest kidney disease is chronic. If kidney size is preserved this might suggest acute renal failure, though some diseases of the kidney are associated with preservation of renal size (examples include diabetic nephropathy and amyloidosis).
What are the absolute indications for acute dialysis?
Absolute indications for dialysis include:
- Hyperkalemia, refractory to medical therapy
- Volume overload/Pulmonary edema, refractory to medical therapy
- Uremic pericarditis
- Uremic encephalopathy
- Severe metabolic acidosis
- Some toxic ingestions