Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

Abstract

Renal lymphatics are abundant in the cortex of the normal kidney but have been largely neglected in discussions around renal diseases. They originate in the substance of the renal lobule as blind-ended initial capillaries, and can either follow the main arteries and veins toward the hilum, or penetrate the capsule to join capsular lymphatics. There are no valves present in interlobular lymphatics, which allows lymph formed in the cortex to exit the kidney in either direction. There are very few lymphatics present in the medulla. Lymph is formed from interstitial fluid in the cortex, and is largely composed of capillary filtrate, but also contains fluid reabsorbed from the tubules. The two main factors that contribute to renal lymph formation are interstitial fluid volume and intra-renal venous pressure. Renal lymphatic dysfunction, defined as a failure of renal lymphatics to adequately drain interstitial fluid, can occur by several mechanisms. Renal lymphatic inflow may be overwhelmed in the setting of raised venous pressure (e.g., cardiac failure) or increased capillary permeability (e.g., systemic inflammatory response syndrome). Similarly, renal lymphatic outflow, at the level of the terminal thoracic duct, may be impaired by raised central venous pressures. Renal lymphatic dysfunction, from any cause, results in renal interstitial edema. Beyond a certain point of edema, intra-renal collecting lymphatics may collapse, further impairing lymphatic drainage. Additionally, in an edematous, tense kidney, lymphatic vessels exiting the kidney via the capsule may become blocked at the exit point. The reciprocal negative influences between renal lymphatic dysfunction and renal interstitial edema are expected to decrease renal function due to pressure changes within the encapsulated kidney, and this mechanism may be important in several common renal conditions.

Lymphatic Programing and Specialization in Hybrid Vessels

“…The AVR in particular is highly fenestrated, lacks mural cell coverage, has a discontinuous basement membrane, and is important for fluid reabsorption back to the vasculature (Figure 1D; Schwartz et al, 1976;Takahashi-Iwanaga, 1991). These features are also attributed to lymphatic vessels which are otherwise absent or rare in the renal medulla (Russell et al, 2019). Similar to SC, the AVR expresses both PROX1 and VEGFR3, but not LYVE1 and PDPN.…”

Lymphatic vessels in solid organ transplantation and immunobiology

“…Renal lymphatics originate from the renal lobule and follow the main arteries or veins toward the hilum. 13 The intrarenal lymphatic system originates from the superficial network, which lines the fibrous capsule. These LVs lack valves, which allows for bidirectional lymph flow, and drain either directly to the hilum, or connect to the deeper cortical lymphatic capillaries that run along the capsular arterial branches.…”

Factors associated with abnormal left ventricular ejection fraction (decreased or increased) in patients with sepsis in the intensive care unit

“…However, there was no significant difference in terms of EF. There is a question as to whether the CVP itself accurately reflects the preload [35,36], and there is no assurance that it has been accurately measured in all patients in this study. Therefore, it cannot be asserted that CVP is not a relevant factor for determining EF in patients with sepsis, and it should be clarified by further studies.…”

“…Central venous pressure (CVP) has been used to assess hemodynamic status, particularly in the ICU [35]. A normal CVP is between 8 to 12 mmHg, this value can be altered by volume status or venous compliance [36,37].…”