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The Kidneys

The kidneys are paired retroperitoneal organs that together receive roughly 20% of cardiac output at rest.[17] In healthy adults, glomeruli can produce as much as 180 L of ultrafiltrate per day.[3] Average urine output is approximately 1.5 L per day.[18]

Kidney anatomy — internal structure and position

OpenStax Anatomy & Physiology — Internal structure of the kidney. (CC BY 4.0)

Surgical Anatomy​

Each adult kidney is approximately 11 × 6 × 3 cm and 125–170 g. The right kidney sits 1–2 cm lower than the left because of the liver. The relations in the operating field are:

AspectLeft kidneyRight kidney
AnteriorStomach, pancreas (body/tail), spleen, splenic flexure, jejunumLiver, duodenum (2nd portion), hepatic flexure
PosteriorDiaphragm, psoas, quadratus lumborum, transversus abdominis; 11th–12th ribsSame; usually only 12th rib
SuperiorLeft adrenalRight adrenal

Upper pole relations explain the risk of pleural injury with posterior flank access above the 12th rib and splenic / hepatic capsule injury during mobilization. Pancreatic tail injury is a recognized pitfall on the left.

Fascial compartments​

The retroperitoneal envelope determines how urinomas track, how abscesses are drained, and which planes are developed during nephrectomy, ureterolysis and auto-transplantation.

  • Renal (fibrous) capsule. The capsule is tightly adherent. It is stripped off in decapsulation and during intraparenchymal dissection or partial nephrectomy.
  • Perirenal fat. This fat immediately surrounds the kidney and harbors accessory polar vessels.
  • Gerota's (renal) fascia. This fascia encloses the kidney, perirenal fat and adrenal. It fuses superolaterally and has limited continuity across the midline; inferiorly, its anterior and posterior leaves merge into a multilaminar fascia in the iliac fossa. Multilaminar caudal renal fascia can restrain perirenal collections, but cadaveric injection studies disagree on communication with the infrarenal and pelvic extraperitoneal spaces; imaging defines the extent of each urinoma or hematoma.[15][27]
  • Pararenal fat. This fat lies outside Gerota's fascia, in anterior and posterior compartments.
  • Transversalis fascia. This fascia forms the lateral limit of the retroperitoneum.

Collecting system​

The papillae drain through approximately 7–14 minor calyces into 2–3 major calyceal groups and then the renal pelvis. Superior and inferior groups are common; an independent interpolar major group is a variant.[28] Calyceal anatomy varies widely and is worth reviewing on preoperative imaging before endopyelotomy, UPJ reconstruction, or percutaneous access planning. The ureteropelvic junction (UPJ) lies on the medial aspect of the pelvis.[5] A lower-pole crossing vessel is a frequent finding in selected adult UPJ-obstruction surgical series.[5]

Innervation and referred pain​

Visceral sensory fibers travel with sympathetic roots T10–L1. Pain from ureteral obstruction, pyelonephritis, or parenchymal distension classically refers to the flank and radiates to the ipsilateral groin or testicle or labium majus, reflecting shared innervation with the genitofemoral and ilioinguinal nerves.

Vascular Anatomy​

Every renal operation is organized around the vascular pedicle.

Renal vascular tree from the renal artery to the glomerular and peritubular capillaries

The renal vascular tree. The renal artery divides into segmental → interlobar → arcuate → interlobular (cortical radiate) arteries, which feed the glomerular afferent arterioles; efferent arterioles then form the peritubular capillary network investing the tubules. (CC BY, OpenStax Anatomy & Physiology)

  • A single renal artery enters each hilum in most people; a systematic review estimated accessory arteries in about 21%, with variation by population and imaging method.[6] Segmental and polar branches often supply distinct territories, so inadvertent loss can cause segmental ischemia; the extent of infarction and whole-kidney functional effect depend on the artery and territory.[7]
  • The main renal artery divides into anterior and posterior branches before or near the hilum, with variable branching.[23] Brödel's plane between these territories is relatively less vascular, varies in extent, and still contains small crossing vessels; it is the classical plane for intersegmental nephrotomy in open surgery.[24] For percutaneous access, a posterior calyceal trajectory helps avoid major vessels but does not eliminate bleeding risk.[25]
  • Arterial branching runs from segmental arteries to interlobar, arcuate (at the corticomedullary junction), interlobular (cortical radial) and afferent arterioles. Efferent arterioles emerging from juxtamedullary glomeruli give rise to the vasa recta that supply the medulla. The medulla is essentially supplied by postglomerular blood and is therefore more vulnerable to ischemia than the cortex.
  • Venous drainage. Interlobular, arcuate, interlobar and segmental veins drain to the main renal vein. The left renal vein usually receives the left gonadal, adrenal, and lumbar veins and crosses anterior to the aorta beneath the SMA, where compression can produce nutcracker physiology. Retroaortic and circumaortic left renal veins are variants to identify on preoperative vascular imaging.[29] The right renal vein is short, drains directly, and usually has no tributaries. A cadaveric morphometric study of 100 kidney pairs measured the right renal vein at 2.4 ± 0.7 cm and the left at 5.9 ± 1.5 cm, a length difference relevant to vascular control during donor nephrectomy, autotransplantation and IVC/renal-vein exposure.[14]
  • Lymphatics. The right kidney drains to right paracaval and interaortocaval nodes and the left kidney to left paraaortic and preaortic nodes. Some cross-drainage occurs between the two sides.

Accessory arteries and reconstruction. Unrecognized variant vessels can complicate renal hilar and UPJ surgery. Review available vascular-phase imaging and, when the operation requires it, map the arteries and veins on both sides, including lower-pole vessels near the UPJ. Preservation or sacrifice of a branch is individualized to its territory, procedure and available reconstruction options; neither CT urogram phase selection nor a brief clamp or Doppler test alone establishes that a segment is dispensable.[6][7]

Nephron Overview (Clinically Relevant Level)​

Each kidney contains roughly a million nephrons, with substantial individual variation. After loss of renal mass, single-nephron filtration can rise in the remaining kidney (compensatory hyperfiltration), but the degree of compensation and long-term outcome vary.[8]

The uriniferous tubule (nephron) and its course through the cortex and medulla

The uriniferous tubule (nephron). The glomerular capsule and convoluted tubules sit in the cortical substance; the loop of Henle descends into the medulla, and the collecting tubules drain through the ducts of Bellini at the papilla. (Public domain, Gray's Anatomy)

Sites of solute reabsorption and secretion along the nephron

Tubular handling along the nephron — the major solutes and water reabsorbed into the blood and secreted into the filtrate at each segment. This segmental division of labor underlies the kidney's clearance of drugs and metabolites and the electrolyte disturbances seen after bowel-segment urinary reconstruction. (CC BY, OpenStax Anatomy & Physiology)

Glomerular filtration depends on three things:

  1. The ultrafiltration coefficient (area × hydraulic permeability of the barrier) falls in glomerulosclerosis, diabetic nephropathy, and with nephron loss.
  2. Ureteral obstruction can raise Bowman's-space pressure and reduce filtration.[16] In rats with partial renal-vein ligation, GFR fell despite an unchanged transglomerular hydrostatic gradient; renal plasma flow and the ultrafiltration coefficient fell while glomerular-capillary and Bowman's-space pressures both rose.[30] Renal tamponade is a proposed contributor to dysfunction in heart failure.[2]
  3. The oncotic pressure opposing filtration is modestly altered by plasma protein concentration.

Tubular function can be collapsed, for operative purposes, into three jobs:

  • Bulk reabsorption (proximal tubule). This segment recovers 60–70% of filtered Na⁺ and water, approximately 80% of filtered bicarbonate, and nearly all filtered glucose, amino acids, and low-molecular-weight proteins.[19][20] Substantial generalized proximal dysfunction can produce low-molecular-weight proteinuria, glucosuria despite euglycemia, aminoaciduria, and phosphaturia (a Fanconi phenotype). These findings are neither consistent nor necessarily early in ischemic or drug-associated acute kidney injury; distinguish injury after contrast from injury caused by contrast.[4][9]
  • Concentration (loop of Henle and collecting duct). This segment generates and exploits the medullary osmotic gradient under vasopressin control. Loop-of-Henle or medullary injury can impair urinary concentration, but post-obstructive diuresis after relief of prolonged obstruction also reflects solute excretion, loss of medullary tonicity, aquaporin downregulation and tubular transporter dysfunction; urine output varies.[16]
  • Fine tuning (distal nephron). The distal nephron regulates final Na⁺, K⁺, H⁺ and water handling under aldosterone and vasopressin, which is relevant when interpreting postoperative electrolyte and acid-base derangements.

The medulla is a vulnerable zone. Its relatively low oxygen tension reflects countercurrent vascular exchange while the thick ascending limb has high transport-related oxygen demand.[1][9] This makes medullary tissue susceptible to hypoxic stress.[1][9] Ischemic, drug-associated and post-contrast kidney injury have different mechanisms and distributions.[1][9]

Illustrative adult reference values​

These approximate values describe healthy adult physiology. GFR, urine volume and concentrating ability vary with age, body size, fluid intake, illness and measurement method.

ParameterTypical adult value
Renal blood flow~1 L/min (20–25% of cardiac output)[21]
GFR~100–125 mL/min/1.73 m² (age-dependent)[22]
Filtration fraction~20%[17]
Daily ultrafiltrate~180 L
Daily urine output~1.0–2.0 L
Minimum urine osmolality~50 mOsm/kg (max dilution)
Maximum urine osmolality~1,200 mOsm/kg (max concentration)

Endocrine Output​

The kidney has three hormonal roles with operative relevance:

  • Renin (juxtaglomerular cells). Reduced afferent-arteriolar perfusion pressure, sympathetic input and reduced distal NaCl delivery trigger renin release. Renin release is relevant in renovascular hypertension, post-clamp ischemic hypertension, and the hemodynamic swings after nephrectomy or revascularization.
  • Erythropoietin (peritubular cortical fibroblasts). Hypoxia stimulates erythropoietin release. Reduced erythropoietin contributes to anemia in advanced CKD over time; an abrupt postoperative hemoglobin fall should not be attributed to new erythropoietin loss without assessing bleeding, dilution and other causes.[10]
  • Active vitamin D (proximal-tubule 1α-hydroxylase). The enzyme converts 25(OH)D to 1,25(OH)₂D. Reduced calcitriol synthesis contributes to secondary hyperparathyroidism and CKD-associated bone disease alongside hypocalcemia and hyperphosphatemia.[31]

Clinical Correlations for the Reconstructive Urologist​

  • Medullary ischemic injury and warm ischemia time. During partial nephrectomy, minimize ischemic exposure while preserving viable parenchyma and achieving safe tumor removal. Some series associate longer warm ischemia beyond about 25–30 minutes with worse operated-kidney function; an off-clamp approach is not routinely superior to limited on-clamp ischemia in patients with two functioning kidneys .[11][12]
  • Segmental arterial supply. Injury to an accessory or polar artery can compromise the supplied territory during partial nephrectomy, donor procurement, transplant, or UPJ reconstruction.[7] The actual infarct and functional consequence depend on branch caliber, territory and collateral or alternative perfusion.[7]
  • Obstruction and backpressure nephropathy. Elevated collecting-system pressure can reduce filtration and injure renal parenchyma. An infected obstructed kidney or obstruction with severe renal failure requires urgent decompression. After drainage, urine output >200 mL/h for at least 2 consecutive hours or >3 L/24 h meets a common definition of post-obstructive diuresis and calls for fluid-balance and electrolyte monitoring, particularly after chronic or bilateral obstruction.[16] Recovery depends on duration, severity, infection, and baseline function.[16]
  • Venous congestion and compartment pressure. Elevated renal venous or intra-abdominal pressure may reduce renal perfusion and filtration; the contribution of a distinct "renal tamponade" mechanism in heart failure remains a hypothesis.[2]
  • Split renal function assessment. MAG3 or DMSA studies can estimate each kidney's contribution when the result would change decisions about a poorly functioning obstructed unit, bilateral disease or salvage versus nephrectomy.
  • Hyperfiltration after nephrectomy. The remaining kidney often compensates, so total GFR usually falls by less than half after donation, but the amount varies between people.[8][13] Donor follow-up includes blood pressure, estimated GFR and albuminuria assessment.[13]
  • Low-molecular-weight proteinuria as a tubular-injury marker. Cystatin C, β₂-microglobulin, and retinol-binding protein are normally reabsorbed by the proximal tubule. Increased urinary excretion suggests impaired proximal reabsorption, but heavy glomerular proteinuria can saturate uptake without primary tubular injury.[4][26]
  • Gerota's fascia, urinoma, and abscess. Urinomas from calyceal tears, pyeloplasty leak, or percutaneous-tract extravasation may be contained within Gerota's fascia; abscesses can cross into the pararenal spaces once Gerota's is violated. Imaging interpretation after any upper-tract reconstruction depends on knowing these compartments.

Videos​

Kidney anatomy
Gross and vascular overview
The nephron
Segmental structure and function
Renal physiology
Filtration, concentration, and regulation

References​

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31. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. "KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD)." Kidney Int Suppl (2011). 2017;7(1):1–59. doi:10.1016/j.kisu.2017.04.001