Kidney Structure


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The kidney is shaped like a kidney bean standing on end. Two layers, the outer renal fascia and an inner capsule, cover the outside of the kidney. The inside of the kidney consists of three layers: the outer cortex, the middle medulla and the inner renal pelvis. The renal pelvis is flush with the concave side of the kidney, and empties into the ureter, a tube that runs down outside the concave side of the kidney. Nine renal pyramids are embedded in the medulla, which is the thickest kidney layer. Each renal pyramid is teardrop-shaped, with the narrow end facing the renal pelvis. The renal artery and renal vein enter the concave part of the kidney, just above the ureter. The renal artery and renal vein branch into arterioles and venuoles, respectively, which extend into the kidney and branch into capillaries in the cortex.

The internal structure of the kidney is shown. (credit: modification of work by NCI)

OpenStax Biology 2e

Externally, the kidneys are surrounded by three layers. The outermost layer is a tough connective tissue layer called the renal fascia. The second layer is called the perirenal fat capsule, which helps anchor the kidneys in place. The third and innermost layer is the renal capsule. Internally, the kidney has three regions—an outer cortex, a medulla in the middle, and the renal pelvis in the region called the hilum of the kidney. The hilum is the concave part of the bean-shape where blood vessels and nerves enter and exit the kidney; it is also the point of exit for the ureters. The renal cortex is granular due to the presence of nephrons—the functional unit of the kidney. The medulla consists of multiple pyramidal tissue masses, called the renal pyramids. In between the pyramids are spaces called renal columns through which the blood vessels pass. The tips of the pyramids, called renal papillae, point toward the renal pelvis. There are, on average, eight renal pyramids in each kidney. The renal pyramids along with the adjoining cortical region are called the lobes of the kidney. The renal pelvis leads to the ureter on the outside of the kidney. On the inside of the kidney, the renal pelvis branches out into two or three extensions called the major calyces, which further branch into the minor calyces. The ureters are urine-bearing tubes that exit the kidney and empty into the urinary bladder.

Because the kidney filters blood, its network of blood vessels is an important component of its structure and function. The arteries, veins, and nerves that supply the kidney enter and exit at the renal hilum. Renal blood supply starts with the branching of the aorta into the renal arteries (which are each named based on the region of the kidney they pass through) and ends with the exiting of the renal veins to join the inferior vena cava. The renal arteries split into several segmental arteries upon entering the kidneys. Each segmental artery splits further into several interlobar arteries and enters the renal columns, which supply the renal lobes. The interlobar arteries split at the junction of the renal cortex and medulla to form the arcuate arteries. The arcuate “bow shaped” arteries form arcs along the base of the medullary pyramids. Cortical radiate arteries, as the name suggests, radiate out from the arcuate arteries. The cortical radiate arteries branch into numerous afferent arterioles, and then enter the capillaries supplying the nephrons. Veins trace the path of the arteries and have similar names, except there are no segmental veins.

The functional unit of the kidney is the nephron. Each kidney is made up of over one million nephrons that dot the renal cortex, giving it a granular appearance when sectioned sagittally. There are two types of nephrons—cortical nephrons (85 percent), which are deep in the renal cortex, and juxtamedullary nephrons (15 percent), which lie in the renal cortex close to the renal medulla. A nephron consists of three parts—a renal corpuscle, a renal tubule, and the associated capillary network, which originates from the cortical radiate arteries.

Illustration shows the nephron, a tube-like structure that begins in the kidney cortex. Here, arterioles converge in a bulb-like structure called the glomerulus, which is partly surrounded by a Bowmans capsule. Afferent arterioles enter the glomerulus, and efferent arterioles leave. The glomerulus empties into the proximal convoluted tubule. A long loop, called the loop of Henle, extends from the proximal convoluted tubule to the inner medulla of the kidney, and then back out to the cortex. There, the loop of Henle joins a distal convoluted tubule. The distal convoluted tubule joins a collecting duct, which travels from the medulla back into the cortex, toward the center of the kidney. Eventually, the contents of the renal pyramid empty into the renal pelvis, and then the ureter.
The nephron is the functional unit of the kidney. The glomerulus and convoluted tubules are located in the kidney cortex, while collecting ducts are located in the pyramids of the medulla. (credit: modification of work by NIDDK)


Clark, M., Douglas, M., Choi, J. Biology 2e. Houston, Texas: OpenStax. Access for free at:

Statins ameliorate cholesterol-induced inflammation and improve AQP2 expression by inhibiting NLRP3 activation in the kidney

Background: Chronic kidney diseases (CKD) are usually associated with dyslipidemia. Statin therapy has been primarily recommended for the prevention of cardiovascular risk in patients with CKD; however, the effects of statins on kidney disease progression remain controversial. This study aims to investigate the effects of statin treatment on renal handling of water in patients and in animals on a high-fat diet. Methods: Retrospective cohort patient data were reviewed and the protein expression levels of aquaporin-2 (AQP2) and NLRP3 inflammasome adaptor ASC were examined in kidney biopsy specimens. The effects of statins on AQP2 and NLRP3 inflammasome components were examined in nlrp3-/- mice, 5/6 nephroectomized (5/6Nx) rats with a high-fat diet (HFD), and in vitroResults: In the retrospective cohort study, serum cholesterol was negatively correlated to eGFR and AQP2 protein expression in the kidney biopsy specimens. Statins exhibited no effect on eGFR but abolished the negative correlation between cholesterol and AQP2 expression. Whilst nlrp3+/+ mice showed an increased urine output and a decreased expression of AQP2 protein after a HFD, which was moderately attenuated in nlrp3 deletion mice with HFD. In 5/6Nx rats on a HFD, atorvastatin markedly decreased the urine output and upregulated the protein expression of AQP2. Cholesterol stimulated the protein expression of NLRP3 inflammasome components ASC, caspase-1 and IL-1β, and decreased AQP2 protein abundance in vitro, which was markedly prevented by statins, likely through the enhancement of ASC speck degradation via autophagy. Conclusion: Serum cholesterol level has a negative correlation with AQP2 protein expression in the kidney biopsy specimens of patients. Statins can ameliorate cholesterol-induced inflammation by promoting the degradation of ASC speck, and improve the expression of aquaporin in the kidneys of animals on a HFD.

Keywords: AQP2; ASC; IL-1β; cholesterol; statins.

Teleological Role of L-2-Hydroxyglutarate Dehydrogenase in the Kidney

L-2-hydroxyglutarate (L-2HG) is an oncometabolite found elevated in renal tumors. However, this molecule may have physiologic roles that extend beyond its association with cancer as L-2HG levels are elevated in response to hypoxia and during Drosophila larval development. L-2HG is known to be metabolized by L-2HG dehydrogenase (L2HGDH), and loss of L2HGDH leads to elevated L-2HG levels. Despite being highly expressed in the kidney, L2HGDH’s role in renal metabolism has not been explored. Here, we report our findings utilizing a novel CRISPR/Cas9 murine knockout model with a specific focus on the role of L2HGDH in the kidney. Histologically, L2hgdh KO kidneys have no demonstrable histologic abnormalities. However, GC/MS metabolomics demonstrates significantly reduced levels of the TCA cycle intermediate succinate in multiple tissues. Isotope labeling studies with [U-13C] glucose demonstrate that restoration of L2HGDH in renal cancer cells (which lowers L-2HG) leads to enhanced incorporation of label into TCA cycle intermediates. Subsequent biochemical studies demonstrate that L-2HG can inhibit the TCA cycle enzyme α-ketoglutarate dehydrogenase. Bioinformatic analysis of mRNA expression data from renal tumors demonstrates that L2HGDH is co-expressed with genes encoding TCA cycle enzymes as well as the gene encoding the transcription factor PGC-1α, which is known to regulate mitochondrial metabolism. Restoration of PGC-1α in renal tumor cells results in increased L2HGDH expression with a concomitant reduction if L-2HG levels. Collectively, our studies provide new insight into the physiologic role for L2HGDH as well as mechanisms that promote L-2HG accumulation in disease states.

Keywords: L-2-Hydroxyglutarate Dehydrogenase; L-2-hydroxyglutarate; PPARG coactivator 1-α; TCA cycle.

Biomarkers of acute kidney injury in patients with nephrotic syndrome

Introduction: Emergence of acute kidney injury (AKI) in patients with nephrotic syndrome (NS) requires prompt diagnosis and differentiation between acute tubular necrosis (ATN) and proliferative glomerulonephritis. We studied the potential use of commercial urinary biomarkers’ tests in the diagnosis of AKI in patients with NS.

Methods: A cross sectional estimate of urinary concentrations of KIM-1 and NGAL was performed in 40 patients with NS: 9 with proliferative glomerulopathy, being 4 with AKI and 31 without proliferative glomerulopathy, being 15 with AKI. AKI was defined using the KDIGO criteria.

Results: The mean age was 35 ± 16 years. The main diagnoses were focal and segmental glomerulosclerosis (10, 25%), membranous glomerulopathy (10, 25%), minimal change disease (7, 18%), lupus nephritis (6, 15%), and proliferative glomerulonephritis (3, 8%). Patients with ATN had higher levels of urinary KIM-1 (P = 0.0157) and NGAL (P = 0.023) than patients without ATN. The urinary concentrations of KIM-1 (P= 0.009) and NGAL (P= 0.002) were higher in patients with AKI than in patients without AKI. Urinary NGAL and KIM-1 levels were significantly higher in patients with ATN without proliferative glomerulonephritis than in patients with proliferative glomerulonephritis (P = 0.003 and P=0.024, respectively).

Conclusions: Neutrophil gelatinase associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) estimates correlated with histological signs of ATN and were able to discriminate patients with AKI even in conditions of NS. Furthermore, urinary levels of NGAL and KIM-1 may be useful in the differential diagnosis of acute tubular necrosis and exudative glomerulonephritis in patients with nephrotic syndrome.

Late outcomes of endovascular aortic stent graft therapy in patients with chronic kidney disease

Endovascular aneurysm repair (EVAR) and thoracic endovascular aortic repair (TEVAR) are effective and minimally invasive treatment options for high-risk surgical candidates. Nevertheless, knowledge about the management of aortic stent graft therapy in chronic kidney disease (CKD) is scarce. This study aimed to examine outcomes after EVAR and TEVAR in patients with CKD.Utilizing data from the Taiwan National Health Insurance Research Database, we retrospectively assessed patients who underwent EVAR and TEVAR therapy between January 1, 2006, and December 31, 2013. Patients were divided into CKD and non-CKD groups. Outcomes were in-hospital mortality, all-cause mortality, readmission, heart failure, and major adverse cardiac and cerebrovascular events.There were 1019 patients in either group after matching. The CKD group had a higher in-hospital mortality rate than the non-CKD group (15.2% vs 8.3%, respectively; odds ratio, 1.92; 95% confidence interval [CI], 1.46-2.54). Patients with CKD had higher risks of all-cause mortality including in-hospital death (46.1% vs 33.1%; hazard ratio [HR], 1.61; 95% CI, 1.35-1.92), readmission rate (62.6% vs 55.0%; subdistribution HR [SHR], 1.61; 95% CI, 1.32-1.69), redo stent (7.8% vs 6.2%; SHR, 1.50; 95% CI, 1.09-2.07), and major adverse cardiac and cerebrovascular events (13.3% vs 8.8%; SHR, 1.50; 95% CI, 1.15-1.95). The subgroup analysis did not demonstrate a variation in mortality between the TEVAR and EVAR cohorts (P for interaction = .725). The dialysis group had higher risks of all-cause mortality and readmission than the CKD without dialysis and non-CKD groups.Among EVAR/TEVAR recipients, CKD was independently associated with higher in-hospital mortality, postoperative complication, and all-cause mortality rates. Patients with end-stage renal disease on dialysis had worse outcomes than those in the CKD non-dialysis and non-CKD groups.

The yin and yang of retinoic acid signaling in kidney diseases

Retinoic acid (RA) signaling is involved in various physiological and pathological conditions, including development, tumorigenesis, inflammation, and tissue damage and repair. In kidneys, the beneficial effect of RA has been reported in multiple disease models, such as glomerulosclerosis, renal fibrosis, and acute kidney injury. In this issue of the JCI, Chen et al. report a pathway activated by RA signaling that is mediated by the retinoic acid receptor responder protein 1 (RARRES1). Specifically, RARRES1, which is proteolytically cleaved to release the extracellular domain, was endocytosed by podocytes to induce apoptosis and glomerular dysfunction kidney disease. These findings unveil the contrasting aspects, a Janus face, of RA signaling that may guide its therapeutic use.

Keywords: structure of kidney, parts of kidney, anatomy of kidney, kidney anatomy, kidney parts, define kidney, what is kidney, explain kidney, research about kidney, kidney research