renal 1
Kidney Anatomy and Position
Kidneys are retroperitoneal, located high in the back and somewhat protected by the ribs.
They are not intraperitoneal; they sit back behind the peritoneal cavity.
The adrenal glands sit on top of each kidney as part of the endocrine system.
The kidney can be conceptually divided into three main regions: cortex (outer, where the nephrons live), medulla (inner region where filtrate flows toward urine collection), and the renal pelvis (central collecting area surrounded by smooth muscle).
The renal pelvis funnels urine into the ureter, which leads to the bladder through which urine is discharged via the urethra.
Kidney transplantation notes:
A transplanted kidney is usually placed in the lower abdomen and may be on the front; the native kidney is typically left in place.
Transplanted kidneys are often not connected with the original nerves, so pain signals from a transplanted kidney may be diminished or absent.
If a patient has a transplanted kidney, consider injuries to that site (lower abdomen) in trauma; pain may come from bleeding or other issues around the transplant.
The transplanted kidney may be at risk during blunt or penetrating trauma since it lacks the protective nerve connections and may not be as protected as the native kidney.
If pain is felt around a transplanted kidney, the cause is not usually the kidney’s nerves, but surrounding structures or bleeding.
Important anatomical terms: urethra (urinating outlet), ureters (tubes from kidneys to bladder).
Clinical takeaway: knowing the kidney, adrenal gland, ureter, bladder, and urethra locations helps in recognizing pain patterns, surgical considerations, and trauma implications.
Kidney Structure and Filtration: The Nephron and Its Parts
Each kidney contains about
\approx 1,000,000
nephrons (in total across both kidneys).The nephron’s core components:
Glomerulus: a blob-like structure that acts as the filtration sieve.
Renal tubule: a long, tubular structure where reabsorption and secretion occur.
Filtration workflow:
Blood enters via renal arteries, branches into smaller vessels that reach the glomeruli.
The glomerulus filters blood; filtrate moves into the renal tubule.
Reabsorption: useful substances are reabsorbed back into the blood.
Secretion: wastes and other substances are moved from blood into the filtrate.
Key waste products handled by the kidneys:
Urea (from ammonia, a byproduct of protein breakdown in liver).
Creatinine (a waste product from muscle metabolism).
Uric acid (from purine metabolism).
Urine formation and composition:
Urine is largely water (about 95%), with the rest being solutes; roughly ~3000 different compounds can be detected in urine.
Albumin is the main protein in urine when proteinuria is present; other proteins may appear in certain conditions.
Leukocytes (white blood cells) in urine can indicate a urinary tract infection (UTI).
Erythrocytes (red blood cells) in urine can indicate bleeding in the urinary tract.
Glucose in urine can indicate diabetes (glucosuria).
Basic physiology of filtration vs reabsorption:
Glomerulus acts as a sieve; the tubule reabsorbs needed substances and can secrete wastes into the filtrate.
Some urea is reabsorbed to aid in osmotic balance; creatinine is largely not reabsorbed (minimal reabsorption).
Urine tends to be more concentrated when water reabsorption is high.
Urine concentration and osmolality:
Concentrated urine has osmolality typically > 500\ \mathrm{mOsm/kg}.
Urine electrolytes:
Urine sodium typically < 20\ \mathrm{mEq/L} in states of renal conservation.
FeNa (fractional excretion of sodium) usually < 1\% in prerenal states.
Hormonal and regulatory roles of the kidneys:
Erythropoietin (EPO): stimulates red blood cell production in bone marrow.
Renin: initiates the renin-angiotensin-aldosterone system (RAAS) to regulate blood pressure and salt-water balance.
Vitamin D activation: kidneys convert vitamin D to its active form.
Blood supply to the kidneys:
The kidneys receive about 25% of cardiac output despite their small size.
Blood reaches the kidneys through renal arteries and branches that become arterioles and interact with nephrons.
Clinical implications:
Reduction in renal blood flow can rapidly degrade filtration and lead to azotemia and other complications.
Nephron Details: Filtration, Reabsorption, and Secretion (Zoomed Views)
Filtration process:
Blood enters the glomerulus where filtration occurs, producing filtrate that enters the tubule.
The glomerulus is a sieve that determines what enters the filtrate.
Reabsorption and secretion:
Substances needed by the body are reabsorbed back into the blood from the tubule.
Waste products are kept in the filtrate and eventually excreted as urine.
A two-panel view (simplified):
Glomerulus (labeled as the filter/SIEVE) with the tubule where reabsorption and secretion occur.
The process is driven by diffusion and osmotic pressure.
Creatinine and urea handling:
Creatinine is largely not reabsorbed; only a tiny amount reabsorbs.
Urea is partly reabsorbed to aid with osmosis and bodily fluid balance.
Clinical note on filtration markers:
A commonly used ratio is the BUN-to-creatinine ratio to assess kidney function and volume status.
Quick test-taker tip:
In normal kidney function, the BUN:creatinine ratio tends to fall within a typical range; deviations can indicate prerenal vs intrarenal etiologies (see AKI section).
Waste Products, Electrolytes, and Urinalysis Indicators
Waste products to monitor:
Urea, creatinine, uric acid.
Urine analysis indicators:
Leukocytes (WBCs): possible UTI.
Erythrocytes (RBCs): possible bleeding within urinary tract.
Glucose: possible diabetes.
Protein/Albumin: proteinuria; may indicate glomerular permeability issues or other conditions (e.g., pregnancy, hypertension, heart failure).
Important clinical concepts:
Albuminuria often reflects glomerular leak; the presence of albumin in urine suggests protein in urine.
There can be a large panel of detectable compounds in urine (thousands), but the major indicators listed help guide initial assessment.
Acute Kidney Injury (AKI): Overview and Time Course
Definition and time course:
AKI = abrupt (rapid) decline in kidney function, typically developing over a few days.
AKI used to be called acute renal failure (ARF).
Chronic kidney injury (CKD) is suggested when kidney dysfunction is present for more than about three months; CKD evolves over a longer timescale.
AKI classification (three broad categories):
Prerenal AKI: due to decreased blood flow to the kidneys (before renal filtration starts).
Postrenal AKI: due to obstruction after the kidneys (urinary outflow obstruction).
Intrarenal AKI: damage within the kidneys themselves (e.g., ischemia, toxins, acute tubular necrosis).
Why AKI matters: the kidneys regulate fluid, waste, electrolytes, and hormones; acute failure disrupts these processes and can be life-threatening if not addressed.
Prerenal AKI: Mechanisms, Causes, and Lab Patterns
Core idea:
Prerenal AKI results from decreased renal perfusion (blood flow) leading to a reduced glomerular filtration rate (GFR).
Causes and scenarios:
Absolute fluid loss: major hemorrhage, vomiting, diarrhea, severe burns (large fluid losses).
Relative fluid loss or reduced effective circulating volume: distributive shock (sepsis, anaphylaxis, neurogenic shock), heart failure with reduced forward flow, dehydration, or conditions causing poor perfusion.
Blocking factors: clots or emboli can reduce renal blood flow; more broadly, anything reducing renal perfusion reduces filtration.
Local renal artery issues: renal artery stenosis or embolus can lower renal perfusion.
Consequences and pathophysiology:
Reduced blood flow to glomeruli lowers GFR; decreased filtration leads to azotemia.
If hypoperfusion persists, renal tissue injury can occur.
Hormonal responses and fluid handling:
Renin release increases, activating RAAS; aldosterone promotes sodium and water reabsorption, maintaining blood pressure and volume.
Antidiuretic hormone (ADH or vasopressin) is released to conserve water.
In prerenal states, there is increased reabsorption of urea (and often sodium and water), which raises the BUN to creatinine ratio.
Laboratory patterns characteristic of prerenal AKI:
GFR is decreased due to low perfusion.
BUN-to-creatinine ratio typically > 20:1 (reflecting preferential reabsorption of urea when perfusion is low).
Formula snippet: \text{BUN/Cr ratio} = \frac{\text{BUN}}{\text{Creatinine}}\quad (\text{normal range } 5:1 \text{ to } 20:1)
Fractional excretion of sodium (FeNa) < 1\% (sodium reabsorption is high to preserve volume):
FeNa formula: \text{FeNa} = \frac{(U{Na} \cdot P{Cr})}{(P{Na} \cdot U{Cr})} \times 100\%,
where U and P denote urine and plasma concentrations, respectively.Urine sodium typically < 20\ \mathrm{mEq/L}.
Urine osmolality typically > 500\ \mathrm{mOsm/kg}, reflecting concentrated urine.
Urine is often darkened due to concentrated solutes and urea.
Oliguria (low urine output) is common; anuria is a complete absence of urine.
Clinical physiology notes:
In hemorrhagic or distributive shock, reduced renal perfusion leads to a rapid drop in GFR and a prerenal pattern if the kidney itself is not damaged.
As perfusion improves (with fluids or treating the underlying cause), kidney function may recover if there is no intrinsic damage.
Additional diagnostic considerations:
Azotemia: elevated nitrogen-containing compounds in the blood, reflected by high BUN and/or creatinine.
The relationship between prerenal AKI and azotemia is due to reduced filtering and preferential reabsorption of urea.
Practical clinical reminders from the lecture:
In prerenal AKI, the kidneys are not damaged per se; they are underperfused, and the problem is upstream of the kidneys.
If the BUN rises disproportionately to creatinine (high BUN/Cr ratio), think prerenal etiology.
Postrenal and Intrarenal AKI: Brief Definitions
Postrenal AKI (obstruction after the kidney):
Obstruction in the urinary tract distal to the kidneys (ureter, bladder, urethra) leading to backpressure and reduced filtration.
Relief of obstruction often improves kidney function if detected early.
Intrarenal AKI (within the kidney):
Includes acute tubular necrosis (ischemic or nephrotoxic), glomerulonephritis, interstitial nephritis, and other intrinsic kidney diseases.
Causes include toxins, severe ischemia, or inflammatory/infiltrative processes.
Additional Concepts Touched in the Lecture
Dialysis context:
For individuals on dialysis, blood is filtered about three times per week (not continuously) to perform the kidneys’ filtration role.
In people with fully functional kidneys, filtration occurs constantly with blood being filtered many times per week (roughly 140–175 times per week, based on activity and metabolic load).
Kidney function and systemic effects:
Renin-angiotensin-aldosterone system (RAAS) activation helps conserve sodium and water during hypoperfusion.
ADH (antidiuretic hormone) also promotes water reabsorption to maintain circulating volume.
Hydrogen ion (H+) handling by kidneys: failure to excrete hydrogen leads to metabolic acidosis, a common consequence of renal failure.
Related conditions and metabolic markers:
Anemia can be a consequence of reduced erythropoietin production in renal failure.
Activation of vitamin D and its downstream effects on calcium and bone health.
Gout and other uric acid–related issues can be associated with renal handling of uric acid.
Urine analysis and interpretation (connection to disease):
Leukocytes in urine suggest UTI; glucose in urine suggests diabetes; erythrocytes indicate bleeding; albumin/protein in urine indicates proteinuria.
SIADH vs Diabetes Insipidus (ADH-related):
SIADH: excessive ADH leading to water retention and concentrated urine; can be caused by brain tumors or trauma.
Diabetes insipidus: insufficient ADH leading to excessive urination and dehydration.
Kidney structure and function recap:
Two kidneys filter a large volume of blood daily, with about 180 L filtered per day (roughly 25 times blood volume per day through the kidneys), enabling robust waste removal and fluid/electrolyte balance.
Quick Reference: Key Numbers and Formulas
Normal BUN/Cr ratio range:
5:1 \leq \frac{\text{BUN}}{\text{Creatinine}} \leq 20:1
Prerenal AKI pattern:
BUN/Cr ratio > 20:1
FeNa < 1\%
Urine Na < 20\ \mathrm{mEq/L}
Urine osmolality > 500\ \mathrm{mOsm/kg}
GFR definition:
The amount of blood filtered by the glomeruli per minute; lower GFR indicates reduced kidney function.
Urine concentration indicators:
Urine osmolality > 500\ \mathrm{mOsm/kg} indicates concentrated urine when water reabsorption is high.
Common daily filtration volume references:
Total filtrate produced daily: roughly 150\text{ to }180\ \text{L/day} (varies by source).
Fully functional kidneys filter the blood about 20–25 times per day (i.e., the entire blood volume is filtered multiple times daily).
Transplant considerations (recap):
Transplanted kidneys sit in the lower abdomen and may lack reconnected pain nerves.
Donor kidney function can allow a person to live well with a single healthy kidney; dialysis is not inferred here but is part of renal failure management.
Summary and Practical Takeaways
The kidneys are essential for fluid balance, waste removal (urea, creatinine, uric acid), electrolyte regulation (notably potassium and sodium), acid-base balance (hydrogen ion handling), and hormonal functions (EPO, renin, vitamin D activation).
AKI is an acute, rapid decline in kidney function, with prerenal, postrenal, and intrarenal etiologies. Prerenal AKI stems from decreased renal perfusion and has distinct lab patterns (elevated BUN/Cr ratio, low FeNa, concentrated urine) that reflect compensatory reabsorption.
A thorough understanding of nephron anatomy (glomerulus and tubule) underpins interpretation of lab values and urinalysis.
Clinical correlations (e.g., UTI signs in urinalysis, evidence of diabetes with glucosuria, proteinuria from glomerular disease, and the importance of monitoring for anemia and acidosis in renal disease) guide evaluation and management in renal emergencies.
In transplantation scenarios, be mindful of altered pain signaling, anatomical placement, and potential trauma considerations for the transplanted organ.