It requires no enormous effort of the intellect to expect a substance to build up in the body fluids when you have disabled that organ which is responsible for its clearance. So with lactate, the loss of enough liver cells will give rise to a lactic acidosis. To a lesser extent, renal failure will diminish the kidney's meager contribution to the task of lactate clearance.
Normally, the rate of hepatic clearance increases linearly with increasing lactate levels; it can increase seven-fold in the context of strenuous exercise, for example. It takes a lot to saturate these mechanisms; however obviously there must be a limit. Consider that if these were perfectly responsive, there would never be any lactic acidosis in a person with a normal liver. Severe lactic acidosis without hepatic dysfunction is actually a rather frequent occurrence, which means that in these situations hepatic and renal clearance mechanisms (though working at a greatly increased capacity) are not coping with the increased rate of lactate production.
Authoritative sources report that the liver received 25% of cardiac output. Of that blood, 75% is supplied by the portal vein. The portal vein also supplies a large portion of the hepatic oxygen demands, 50-60%. If hepatic blood flow is decreased significantly, the rate of lactate clearance begins to suffer- predominantly because the lactate is not being delivered to the periportal hepatocytes. Then, if you also decrease hepatic oxygenation, the liver is forced to survive on anaerobic glycolysis. This creates the unusual problem where it could become a source of lactate, rather than the method of its clearance.
Exactly how little blood flow is required seems to be rather individual, but animal data seems to suggest that the liver will battle against lactate until the last drop of blood. Using isolated pig livers, Johnson et al (1976) found that, as long as about 100ml/min of well oxygenated blood was arriving via the hepatic artery, the liver would continue to metabolise exogenous lactate, and would not become a net producer of lactate unless the total blood flow decreased to below 75 ml/min, or about 11ml/100g/min. For perspective, the most widely quoted liver shock factoid is that hepatic blood flow can fall to to 25% of its baseline values and still be compatible with survival (this seems to originate from an old animal model of haemorrhagic shock by Bounous et al, 1963). That would still correspond to a total blood flow of around 300ml/min in the adult human, which means under most normal circumstances the liver of the trauma patient is not acting as a lactate producer.
Yes, this is a page about lactic acidosis as a result of hepatic insufficiency, but the kidneys merit a mention. There is a “lactate threshold” for proximal tubular resorption of lactate. One must remember that lactate is normally a useful participant in the Cori cycle. If it were allowed to constantly leak out via the nephron, it would result in a constant loss of fuel, and so (like glucose) at normal concentrations the proximal tubule is very efficient at retrieving it from the tubular lumen.
At concentrations above 5-6mmol/L, the kidney begins to leak lactate into the urine, and so only in situations of severe lactic acidosis does this clearance mechanism begin to play a significant role.
However, under normal conditions the kidney is also responsible for some proportion of lactate clearance by metabolism (back into glucose) – approximately 15% of it, if dog kidneys are anything to go by. The renal cortex is responsible for this; the medulla on the other hand is a lactate-producing organ which relies on the Cori cycle.