The general question "why is this patient passing no urine" comes up rather frequently in the vivas, hot cases and life in general.
Previous SAQs on this topic:
What do you call "oliguria"? Well, a few definitions exist.
If one were to hang one's reputation on a single definition, one could do worse than ADQI (2004):
Oliguria is a urine output less than 0.3 mL/kg per hour for at least 24 hours.
Oliguria suggests that either the glomerular filtration rate has decreased catastrophically, or there is some sort of mechanical obstruction to urine flow.
In brief, the causes are:
- Decreased intravascular volume (thus decreased renal perfusion)
- Decreased renal perfusion with normal volume (eg. sepsis or other sorts of distributive shock)
- Renal vascular insufficiency (including microvascular vasoconstriction, eg. by ACE-inhibitors)
- Acute tubular necrosis
- Mechanical urinary tract obstruction
Causes of acute renal failure are listed in another chapter, but one ought to be reminded that not all renal failure needs to be oliguric.
This is vaguely in order, and if one were inclined towards building flowcharts one might even try to arrange this into one. However, there is no discrete starting point, and one might skip steps or introduce extra steps, so in real clinical life the progression throught his algorithm is seldom linear. Instead, one might have to generate a generic-looking diagnostic approach like this if one were asked to "discuss the investigations and management of acute renal failure in the ICU".
Rule out mechanical obstruction
- Explore the IDC (is it blocked?)
- Perform a renal tract ultrasound
- One may need to progress to a CT-KUB to assess the cause of the obstruction (eg. calculus, tumour, trauma, and so forth)
Distinguish pre-renal from intra-renal causes on the basis of biochemical indices
- The biochemical differences between pre-renal and intra-renal failure are explored in greater detail in another chapter. Briefly:
- Pre-renal failure is associated with concentrated urine, a disproportionately elevated serum urea, a low fractional sodium excretion and a low urine sodium
- Intra-renal failure (ATN) is associated with more dilute urine, a normal urea-creatinine ratio, a normal fractional sodium excretion and a high urine sodium.
Exclude obvious causes of pre-renal failure
- Hypovolemia, hypotension - basically, the shock states.
- It may be wise to consider premorbid blood pressure norms. If the patient is normally hypertensive, it makes no sense to maintain their MAP at 65mmHg, and one may wish to aim higher (there is some evidence that a higher MAP target may be nephroprotective).
- Abdominal compartment syndrome (one may wish to measure the pressure)
- Renal vascular disease (one may wish to perform renal doppler studies to exclude renal artery stenosis or renal vein thrombosis)
Explore the intra-renal differentials
- Renal failure history (i.e. how damaged were the kidneys before all this)
- Drug history (nephrotoxins, antibiotics, NSAIDs, ACE-Is, etc)
- Nephrounfriendly past medical history (hypertension, diabetes, etc)
- Travel history (being eating weird Swedish sausage?)
- Family history (eg. polycystic kidney disease)
- Social / occupational history (solvent abuse, or merely work-related exposure?)
- Recent infections / exposure (eg. strep throat, enteritis, etc)
- Autoimmune weirdness (myalgias, GI motility issues, joint aches, random rash, haemoptysis)
- Volume assessment
- Oedema, pulmonary or otherwise
- Renal exam
- Ballottability, kidney size (polycystic?)
- Flank tenderness (pyelonephritis?)
- Renal artery bruits
- Search for other contributing diseases
- Cardiovascular exam for heart failure
- Abdominal exam for liver failure, ascites, splenomegaly (malignancy)
- Search for systemic features of autoimmune disease
- Rash (eg. lupus, dermatomyositis)
- Muscle swelling/tenderness
- Lymphadenopathy (malignancy)
- Urine examination
- culture the urine, obviously
- Urine protein analysis (light chains)
- Bloods for differentials
- Blood film (MAHA)
- ADAMTS13 (TTP/HUS)
- EPG/IEPG (multiple myeloma)
- Eosinophil count (interstitial nephritis)
- CK level (would be embarrassing to miss rhabdomyolysis)
- Bloods for immunology
- Anti-C1q, IgG, ASOT (for streptococcal GN)
- Anti-GBM, ANCA (Goodpastures)
- Anti-MPO, PR3 (ANCA-positive GN)
- Anti-dsDNA, C3, C4, antiphospholipid (lupus)
- Streptococcal serology
- Examine the urinary sediment
- Hyaline casts are not associated with anything specific
- Fatty and waxy casts are suggestive of long-standing renal disease, whatever its cause.
- Muddy brown (coarse granular) casts and tubular epithelial casts are associated with ATN
- Red blood cell casts indicate glomerular disease
- Shredded-looking RBC fragments also indicate glomerular disease
- Intact-looking red cells suggest some source of bleeding inside the urinary tract, eg. calculi trauma, malignancy, or the haemorrhagic cystitis of cyclophosphamide therapy.
- Eosinophils in the urine, especially when they comprise in excess of 5% of the total urinary WCCs, may suggest acute interstitial nephritis
- White cells in excess, and white cell casts specifically, suggest pyelonephritis - but not in the neutropenic patient. Among neutropenic children with UTI, Klaassen et al (2011) found only 4% had leukocytes in the urine, as compared to 68% of non-neutropenic controls.
- Nitrites will still be present even if the patient is neutropenic, as they are a product of bacterial metabolism (specifically nitrate reductase activity, which is mostly a feature of gram-negative bacteria).
- Pigmented casts may suggest myoglobin as the cause of ATN
- Urinary myoglobin levels confirm rhabdomyolysis
- Urinary crystals suggest some sort of crystalline nephropathy (they might be urate, oxalate, sulfonamides, etc)
- Ultrasound (renal artery stenosis, rebnal vein thrombosis, parenchyma, and obviously pelvocalyceal diltataion)
- CT KUB (to rule out renal calculi and hydronephrosis/pyelonephritis)
- When all else fails
- A renal biopsy may yield diagnostic information, provided one manages to biopsy something relevant. Potentially, one's sample could be full of uselessly necrotic parenchyma, which all looks the same (therefore there will still be no diagnosis, and now one's patient has a hole in their kidney).